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 GUYTON'S DIAGRAM BROUGHT TO LIFE – FROM
GRAPHIC CHART TO SIMULATION MODEL FOR
TEACHING PHYSIOLOGY
Jiří Kofránek, Jan Rusz, Stanislav Matoušek
Laboratory of Biocybernetics, Department of Pathophysiology, 1st Faculty of Medicine, Charles
University, Prague, Czech Republic

Abstract
Thirty five years ago, A.C. Guyton et al. published a description of a large model of
physiological regulation in a form of a graphic schematic diagram. The authors
brought this old large-scale diagram to life using Matlab/Simulink. The original
layout, connections and description of individual blocks were saved. However,
contrary to the old system analysis diagram, the new one is also a functional
simulation model by itself, giving the user a possibility to study behaviour of all the
variables in time. Furthermore, obvious and less obvious errors and omissions were
corrected in the new Simulink diagram.

1 Introduction
Prof. Arthur C. Guyton, T. G. Coleman and H. J.
Grand published the article [6] in the Annual Review
of Physiology magazine 35 years ago. It was a
completely different form of article than usual
physiological articles published until that time. Its
fundament was a large scheme, which at first sight
evoked some electrotechnical device, but there were
computing blocks shown (multipliers, dividers,
summators, integrators, functional blocks) instead of
electrotechnical components. They symbolized
mathematical operations, which were applied on
physiological quantities. Connecting wires between
blocks represented complicated feedback connections Figure 1: Dr. Arthur C. Guyton, with
of physiological quantifiers? Blocks were divided to medical students discussing his computer
eighteen groups, which have represented separate model of cardiovascular system.
physiological subsystems. The central subsystem
symbolized circulation dynamics – to which other blocks were connected (kidney, tissue fluid,
electrolytes, hormonal control and autonomous nervous regulation) via feedback connections..

2 Schematic Diagram Instead of Verbal Description

The article described a large-scale model of the circulatory system regulation in wider
perspective: The respiratory system is integrated into other subsystems of the organism that influence
its function. Instead of giving the reader a set of mathematic equations, the article uses fully equivalent
graphical representation. This syntax graphically illustrates the mathematical relationships in the form
of the above mentioned blocks. The description of the model was given in the form of a principal
graphical chart only (which was, however, fully illustrative), explicatory comments and reasoning
behind the given formulas were very brief, e.g.: “Blocks 266 through 270 calculate the effect of cell
pO2, autonomic stimulation, and basic rate of oxygen consumption by the tissues on the actual rate of
oxygen consumption by the tissues.” Such a formulation required full concentration, as well as some
physiological and mathematical knowledge for the reader to understand the meaning of the formalized
relationships between the physiological entities. Later, in 1973, and in 1975 Arthur C. Guyton
published monographs [7,8], where he explained most of the concepts in more length.
Guyton’s model represents the first large-scale mathematical description of the body's
interconnected subsystems and their functioning. It was indeed a turning point – the impetus to start

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 Technical Computing Prague 2007. 15th Annual Conference Proceedings. Prague, 2007

Figure 2: Overall regulation model of Circulation - original scheme by A.C.Guyton et al., 1972.
Reprinted, with permission, from the Annual Review of Physiology, Volume 34 (c)1972 by Annual
Reviews www.annualreviews.org

the research in the field known as integrative physiology. Using the system analysis of the
physiological regulation, the model was for the first time in history able to depict the simultaneous
dynamics of the circulatory, excretory, respiratory and homeostatic regulation.
The group of A. C. Guyton kept upgrading and extending the model later on, and upon request
they even provided the FORTRAN source code of the model realization to the ones interested. In
1982, the “Human” model appeared [4], representing yet another milestone in the simulation model
development. It gave the possibility to simulate a number of pathological conditions on a virtual
patient (cardiac, respiratory, kidney failure, etc.) and the therapeutic influence of various drugs,
infusions of electrolytes, blood transfusion, etc. Furthermore, the effect of the artificial organ use on
normal physiological functions could have been simulated (artificial heart, artificial ventilator,
dialysis, etc.). Its current interactive web implementation is available from this
addresshttp://venus.skidmore.edu/human.
The latest work results from Guyton's colleagues and students are Quantitative Circulatory
Physiology and Quantitative Human Physiology simulators [1]. Models can be downloaded from this
address http://physiology.umc.edu/themodelingworkshop/.

3 Pioneer of the Systemic Approach in Physiology

Arthur C. Guyton (Fig. 1) was among the pioneers of system analysis in the inquiry of
physiological regulation. He introduced many fundamental concepts regarding short and long time
regulation of the circulation and its connection with the regulation of circulating volume, osmolarity
and ionic composition of bodily fluids. He worked up a great many original experimental procedures –
for instance, he was the first one to measure the value of pressure in the interstitial fluid. However, he
was not only an innovative experimenter, but also a brilliant analyst and creative synthesizer. He was
able to draw out new conclusions for the dynamics of processes in the body from the experimental

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 ISBN 987-80-7080-658-6, CD ROM Proceedings, http://www.humusoft.cz/akce/matlab07
results and thus explain the physiological basis of a number of regulatory processes in the organism as
a whole. Guyton’s research has shown, for example, that it is not only the heart as a pump that
controls the cardiac output; but that an equally important roles are played by the regulation of tissue
perfusion, dependent on the oxygen supply, as well as on the filling of the vessels and the compliance
of great veins. It was A.C. Guyton who proved that the long-term regulation of blood pressure is done
by kidneys [9].
When you study the dynamism of regulatory processes, verbal description and
common sense are often not sufficient. Prof. Guyton realized this already in the mid sixties, when
he studied the factors influencing blood pressure. Hence, he has searched a more exact way of
expressing relationships; first using connected graphs and finally also computer models. He created
his first computer models, together with his long-term colleague Thomas Coleman, in 1966. As an
erudite physiologist and a hand-minded person at the same time, he was engaged in biomedical
engineering in times, when this specialization did not yet officially exist.

Remarkably, Guyton did not intend to engage in theoretical medicine at first. His original aim
was to work in the clinical field. After he graduated from Harvard University in 1943, he began his
surgical internship at Massachusetts General Hospital. His surgical carrier was interrupted by war. He
was called into the Navy. However, he worked in bacteriological warfare research during most of this
period. After the war, he returned to the surgery, but only for a short while. In 1946, overworked, he
suffered a bout of poliomyelitis that left serious consequences – paralysis of the left arm and leg had
bound him either to a wheelchair or crutches for the rest of his life. However, his creative spirit did not
leave him in this period of hardship, and he invented an electric wheelchair controlled by “a joystick”,
as well as a special hoist for easy transfer of disabled people from bed to the wheelchair. Later, he
received a Presidential Citation for his invention. The physical handicap ended Guyton’s carrier in
cardiac surgery and steered him into the theoretical research. In spite of having job offers at Harvard
University, he returned back to his hometown Oxford, Mississippi, where he first taught pharmacology
at a two-year medical school; however, not long after that, he became head of the Department of
Physiology at The University of Mississippi. He established a world famous physiological school in
what used to be a rather provincial institute (on an American scale). Here, he wrote his world-famous
textbook of physiology, originally a monograph that has seen its eleventh edition already, as well as
more than 600 articles and 40 other books. He has trained many generations of medical students and
more than 150 Ph.D. students. In 1989, he passed on the leadership of the institute to his disciple J.E.
Hall and as a professor emeritus devoted himself to research and teaching. He died tragically in an
automobile accident in 2003.

4 Fixing Errors in Guyton's Chart

Guyton was among the first proponents of the formalized description of physiological reality.
Formalization means converting a purely verbal description of a relevant array of relationships into a
description in the formalized language of mathematics. Guyton's diagram from 1972 (Fig 2) is a
formalized description of results of one of the first significant systemic analysis of physiological
functions.
Graphic notation for description of quantitative and structural relations in physiological systems
suggested by Guyton was adopted by other authors in the seventies and eighties. For example, in 1977
[2] they used a slightly modified Guyton's notation in their monograph, covering the system analysis
of interconnection between physiological regulation systems, [11] formulated, in Guyton's notation,
their model of overall regulation of body fluids, etc.
Later on, means of simulation development tools were used for graphic notation of the structure
of physiological regulation relations, for example; Simulink by the Mathworks company or open
source free software package for teaching physiological modelling and research JSIM [16, 17] (see
http://www.physiome.org/jsim/), or recently, graphic means of expression of simulation language
Modelica [5].
Simulink diagrams are very similar to the thirty five year old notation used in the original model
of A.C.Guyton. Therefore we decided to revive the old model by means of a modern software
instrument. We tried to keep the resemblance identical as it was in the original pictorial diagram - the
layout, the disposition of wires and the quantity labels are the same.

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 Technical Computing Prague 2007. 15th Annual Conference Proceedings. Prague, 2007

5 6
3.257
QAO DVS VVS
5
+ 0
QVO

5 6
3.257
QAO DVS VVS
5 + 0
QVO

Corrected

Figure 3: The error in the Circulatory Dynamics subsystem.

The realization of the old diagram is not as smooth as it might seem at first sight, because, there
are errors and omissions in the original scheme. In a hand-drawn picture, it does not matter so much,
because the overall meaning is still valid (most of the errors are present just on the paper, not in the
original FORTRAN implementation). However, if we try to bring the model to life in Simulink, the
errors show up. The model either behaves inadequately or even becomes unstable, values start to
oscillate and the model complex collapses. There were a few errors – changed signs, a multiplier
instead of a divider, changed connection between blocks, missing decimal point, wrong initial
conditions, etc. – but it was enough for a wrong functioning of the model. Being acquainted with
physiology and system analysis, we could have avoided the mistakes with a little effort.
An easily detectable error in the diagram is, for instance, wrong marking of flow direction in the
summation block no. 5 in subsystem Circulatory Dynamics (Fig 3). It is obvious, that the rate of
increase in systemic venous vascular blood volume (DVS) is the subtraction (not the summation)
between all rates of inflows and rates of outflows. Inflow is a blood flow from systemic arterial system
– its rate is denoted as QAO, outflow rate from systemic veins is a blood flow rate from veins into the
right atrium (QVO). The rate
change of filling of the
vascular system as the blood
volume changes (VBD) is
calculated from the difference
between summation of overall
capacity of vascular blood
+ compartments and blood
volume – therefore VBD is the
outflow rate and not the inflow
rate, and in the summator it
must have a negative sign.
In subsystem Non-
Muscle Oxygen Delivery,
+ there is a wrong depiction of
connection in integrative block
Corrected no. 260 (Fig.4). If the model
was programmed exactly as
Figure 4: The error in the Non-Muscle Oxygen Delivery subsystem. depicted in the original

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 ISBN 987-80-7080-658-6, CD ROM Proceedings, http://www.humusoft.cz/akce/matlab07

VIE
1.5
337

HKM

HM2
1600
336 HMK

40 HM

RC1
331
+
+ VIE VIE
1.5 1.5
0 337 337
RCD
332

HKM HKM
1600
0.8 HM2 90
HM2 HMK
336 336
HMK
50 +
RC1
331 40 -
+
- 0 40 HM
40
0 -
RCD +
332
40 HM

Corrected (A) Corrected (B)

Corrected
Figure 5: The errors in the Red Cells and Viscosity subsystem.

diagram, the value of non-muscle venous oxygen saturation (OSV) would constantly rise and the
model would become unstable very quickly. Besides, there would be an algebraic loop in the model.
Correction is simple, input to summator no. 258 is the value of OSV, and therefore it is sufficient to
move feedback input to summator behind the integrator as it is indicated in the picture.
Small and simple subsystem Red Cells and Viscosity includes two errors (Fig 5). The first is
visible at first sight. It is obvious that the rate of change of red cell mass (RCD) is the subtraction (not
the summation) between red cell mass production rate (RC1) and red cell mass destruction rate (RC2).
The second error is obvious as well. During calculation of a portion of the blood viscosity caused by
red blood cells (VIE) from value of hematocrit (HK) according to the diagram, the viscosity would
have to constantly rise, because the value of quantity HM2 would incessantly rise (HK is the input to
the integrator). According to the diagram, the value of a variable HM2 is equal to 1600 - in a stable
situation and under normal conditions. If we divide this value by a constant parameter HKM
(=0.000920), we should arrive at a normal value VIE. Normal value VIE should be 1.5 (formulated as
a ratio to viscosity of water). We can find out, by simple calculation, that it is not so, and we will
arrive at the correct calculation if we multiply the value HM2 by constant HKM instead of using
division. Thus it is obvious, that block no. 337 should be a multiplier unit and not a dividing unit. In
order to have the value of a variable HM2 in stable situation constant (and under normal conditions
equal to value 1600), the input to integrator must have zero value (block no. 336). Therefore, it is
apparent, that the depiction of feedback has been omitted in the diagram. The corrected diagram is
shown in picture 6 as "Corrected (A)". Viscosity is proportionate to hematocrit and the integrator acts
here as a dampening element. It can be from the experimental data that dependence of viscosity of
blood on hematocrit is not linear proportionate [7]. Therefore in a later realization of the model
(according to source text in Fortran language) the relation between hematocrit (HK) and portion of
blood viscosity was caused by red blood cells (VIE) formulated as follows:
HM
VIE = (1)
( HMK − HM ) HKM

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 Technical Computing Prague 2007. 15th Annual Conference Proceedings. Prague, 2007

1
AHC
185
158A

.3333 .14
183 184
AH 1
+

1 AHC

185

158A

.3333 .14
183 184
AH 1
+

Corrected
Figure 6: The error in the Antidiuretic Hormone Control subsystem.

Where:
HMK = 90
and
HKM = 5.3333
which is shown in a diagram in fig. 6, marked as Corrected (B). If we compare this picture with the
original chart, the integrator no. 336 is replaced with dividing and summator units (and the value of
HKM constant is quite different). Maybe, this exact structure should have been originally drawn in the
original diagram, and (by mistake, the integrator was drawn instead of divider and summator) a label
HKM on the left side next to integrator no. 336 indicates this situation.
An error in Antidiuretic Hormone Control subsystem is not visible at first sight (Fig. 6).
According to graphic diagram, the following should hold true:
During stable conditions, according to data on the graphic diagram under normal conditions,
the values should be: :
0.333 AH = 1 ,
AHC = 1 .
Then the integrator 185 will have no zero value and the system will not be in stable condition.
Where is the error?
AH*0.3333 is a normalized rate of antidiuretic hormone creation (ratio of current rate of
creation according to the norm). AHC is a normalized concentration of this hormone (according to the
norm). How is the normalized concentration of substance from normalized rate of substance creation
calculated? The classic compartment approach will answer our question.
In subsystems of conducting ADH creation, aldosterone and angiotensin are calculated in the
model from the rate of hormone inflow (normalized as a relative number according to the norm) and
hormone concentration (again normalized as a relative number according to the norm).

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 ISBN 987-80-7080-658-6, CD ROM Proceedings, http://www.humusoft.cz/akce/matlab07
We come out of a simple compartment approach - into a whole-body compartment inflow the
hormone at the rate Fi (it is synthesised) and outflows at the rate Fo. Quantity of hormone M in whole-
body compartment depends on the balance between inflow and outflow of the hormone.
dM
Fi − Fo = . (2)
dt
Rate of depletion of hormone Fo is proportional to its concentration c:
Fo = k c . (3)
Concentration of hormone c depends on overall quantity of hormone M and on the capacity of
distribution area V:
M
c= . (4)
V
Thus after inserting:
k M dM
Fi − = . (5)
V dt
Provided that the capacity of distribution area V is constant, we will substitute ratio k/V for
constant k1:
k
k1 = . (6)
V
We arrive at:
dM
Fi − k1 M = . (7)
dt
In the model, Guyton calculated the concentration of hormone c0 normalized as a ratio of
current concentration c to its normal value cnorm:
c
c0 =
cnorm . (8)

At invariable distribution area V ratio of concentrations is the same as a ratio of current overall
quantity of hormone M to overall quantity of hormone under normal conditions Mnorm:

c M
c0 = =
cnorm M norm
. (9)
If we formulate the rate of flows in a normalized way (as a ratio to normal rate), then under
normal conditions:
Fi = 1 ,
dM norm
=0.
dt
Therefore:
1 − k1 M norm = 0 . (10)
Normal quantity of hormone Mnorm will be:
1
M norm =
k1 . (11)

Hence, the relative concentration of hormone c0 can be formulated:

M
c0 = = k1 M . (12)
M norm

Thus:
c0
M=
k1 . (13)

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 Technical Computing Prague 2007. 15th Annual Conference Proceedings. Prague, 2007
After inserting into differential equation we arrive at:
⎛c ⎞
d ⎜⎜ 0 ⎟⎟
c k
Fi − k1 0 = ⎝ 1 ⎠ , (14)
k1 dt

i.e.:
⎛ 1 ⎞ dc
Fi − c0 = ⎜⎜ ⎟⎟ 0 . (15)
⎝ k1 ⎠ dt
Thus:
(Fi − c0 )k1 = dc0 . (16)
dt
According to this equation, the normalized concentration of the hormone c0 is calculated from
the normalized inflow of the hormone Fi. In original Guyton's chart, the normalized concentration of
aldosterone and angiotensin is calculated in this way. In case of ADH, there is an error in the chart.
The normalized rate of inflow in case of ADH:
Fi = 0.3333 AH . (17)
The normalized concentration of the hormone is:
c0 = AHC , (18)
Coefficient k1 = 0.14 .
dc0 dc
Instead of (Fi − c0 )k1 = , there is a graphic representation of relation Fi − c0 k1 = 0 .
dt dt
Correct relation in case of ADH should be:
(0.3333 AH − AHC )0.14 = dAHC . (19)
dt
This relation corresponds to a correct part of diagram shown in fig. 6
Quoted examples of errors in the original graphic depiction of Guyton's model do not mean at
all that the actual implementation of the model did include the above-mentioned errors. The model
was implemented in Fortran language and it functioned flawlessly. What was incorrect was only the
graphic depiction of the mathematical relations that did not correspond to the model.
If somebody implemented the model exactly according to the depiction, without thinking over
and understanding the meaning of mathematical relations between physiological quantities, then such
a model would not function correctly on a computer.
It is interesting, that this complicated schematic diagram was many times overprinted in several
publications and nobody made an effort to fix these errors. After all, at the time, when picture schemes
were created, no appropriate application had existed yet – pictures arose like a complicated drawing –
and to handle redoing such a complicated drawing isn’t so easy. Maybe the authors didn't even want to
correct the errors – the ones who took the pain over the analysis of the model easily uncovered the
diagrams mistakes, the ones who just wanted to blindly copy, failed.
After all, at that time, the authors even used to send round the program source files in Fortran
language, so if somebody wanted to just test the behaviour of the model, s/he did not have to program
anything (at the most they had to routinely convert the Fortran program into other programming
languages).

5 Results
After the correction of errors in the original Guyton's chart, we realized its Simulink
implementation. In the Simulink diagram, we tried to maintain the same distribution of all the
individual elements, as in the original diagram.

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 ISBN 987-80-7080-658-6, CD ROM Proceedings, http://www.humusoft.cz/akce/matlab07
The only difference is in the graphic shapes of the individual elements - e.g. in Simulink, the
multiplier/ divider is represented as a square unlike the "piggy" symbol in Guyton's notation (See Fig.
7). The integrator does not have the sign of integral on itself but the expression "1/ s" (being related to
the transcription of Laplace transformation).
In the Simulink model, we also used switches, by which we could couple or uncouple individual
subsystems and control loops.
Resultant chart of Simulink model is depicted in Fig 8.
We can transform individual physiological subsystems of the model into the form of Simulink
subsystems. The graphic chart of the whole model looks rather better arranged (Fig. 9). Then the
diagram of the model resembles the interconnected network of electronic chips – instead of electric
signals; however, there is a flow of information in individual conductors - data of the model.
Physiological subsystems are represented by "simulation chips" – conductors with input data are
connected to their individual input, and signals with information about the value of individual
physiological quantities are distributed from their output “pins” to other “simulation chips”.
Models formulated through the network of "simulation chips" are also the appropriate tools for
team collaboration between branches of study [13]. Such a chart is much more legible also for an
experimental physiologist who does not have to understand the complicated mathematical structure of
a computational network inside a "simulation chip", however s/he understands the structure and
functions of physiological relations. S/he can study the behaviour of a model in individual simulation
chips on virtual displays and oscilloscopes, which are standard components of the Simulink
environment.
In fig. 10, there is a Simulink implementation of a Guyton-Coleman model from 1986,
formulated with the help of interconnected "simulation chips". When the reader compares it to a
previous picture, s/he can imagine how the model has expanded in the past 14 years.

NON-MUSCLE OXYGEN DELIVERY

260

1
57.14
02M s xo
OSV 0.7 259
168
269 AOM 261

1 270 POV
5
+ 258
- +
268 262
POT

+
257
RDO
2688
512 2 POV
267 lower limit 50 263
5

u^3 P40^3

DOB
256
264
266 P4O
MO2
8.0001
265 2400

271
u^3 POT^3 255
xo
271
1
s BFN
1 HM

upper limit 8 272

QO2 OVA
P1O POT
0.00333

3 BFN

1 POT
4
AOM

Figure 7: The pictorial block scheme of the original A.C.Guyton's model on the left and the model
block diagram in the Simulink software tool. Analogically positioned and numbered blocks represent
the same mathematical operations. Multipliers and dividers: blocks 255, 257, 259, 261, 263, 268 ,272,
270 ; sum blocks: 256, 258, 262, 264, 266, 269; integrator blocks: 260 a 271; function blocks (cubic
function): 265 a 267; high level saturation: between blocks 272 and 286, low level saturation:
between blocks 265 and 180. The switches can either be set to receive the input values from other
subsystems, or directly from the user, thus disconnecting the block from the rest of the model.

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 Technical Computing Prague 2007. 15th Annual Conference Proceedings. Prague, 2007
.

NON-MUSCLE OXYGEN DELIVERY MUSCLE BLOOD FLOW CONTROL AND PO2

260
228 240 PM3
1 1 BFM PK2 245
57.14
02M OSV s xo 259 PMO AU 254
0.7 800 AMM
1
168 1
269 AOM 261 227 1
229 lower limit .001
s xo
1 POV 5 239 237 02A
270 RMO
5 PK1 PK3 0.15
258 1 1
2500 PM1^2 u^2 253

226 246
268 262
POT 40 230 5
236
POV OVA 238 QOM PM4
257 0.25
RDO 40 198.7 -1
2688 BFM 1
s xo 252
512 247
267 lower limit 50 263 P2O AOM
5 0.7 1
OVA 231 2400 8
x 235 POE
u^3 P40^3 225 200 1 o Xo P2O 1
upper limit 8
s
DOB 7.983 lower limit .005
256
264
266 P4O 5 DVS 248 251
MO2 241
1
8.0001 RMO 8.0001
265 2400 232 57.14
224 OSA 60
271 234
u^3 POT^3 HM 255
xo 1
271 P3O
1 242 250
s PVO 244
BFN OVA
40 223 P3O^3 u^3 1
272 233 POM
upper limit 8
QO2 200
P1O POT 0.00333 0.08
PM5 PDO
243
122
2.8 PMO 249
2.859 0.5 8
8 512 EXC
VPF 40
HM 1
POT 0.0125
40 PVO
8

0.9999
AOM

1 0.9864
AMM

NON-MUSCLE OXYGEN DELIVERY MUSCLE BLOOD FLOW CONTROL AND PO2 VASCULAR KIDNEY DYNAMICS AND EXCRETION
260
STRESS THIRST AND DRINKING
228 240 PM3
1 1 BFM PK2 245 RR GFN
02M
57.14
OSV
s xo 0.7 259 800
PMO AU 254 AMM
RELAXATION 206 218
8 POT
192 193 194
1 205 GFR VUD STH
168 1
269 AOM 261 227 200
1
229 lower limit .001 65 VUD 1
s xo lower limit 0.0003 STH TVD
POV 239 237 02A 0.125 0.001 8.25 4
1 270 5 1 0.001022 lower limit 0
RMO PK1 PK3 208 1
5 0.15 s Z10 Z11
258 1 1 0.00781 0
2500 PM1^2 u^2 253
EVR PFL
246 199 190 191
268 226 TRR AHM
262 64 0.8 1
POT 230 AAR
40 5
236 VV7 212 TVD
OVA 238 QOM PM4 1000 0.01
POV
257 0.25 0 AAR 0.0009964
RDO -1 198 PPC 209 219
40 198.7 BFM 1 SRK 51.66 0.009
2688 217
s xo 252 33 18 1
512 247 GLP
267 lower limit 50 263 P2O AOM VV6 63
5 0.7 1
OVA 231 2400 8 5
xo 235 Xo POE VV7 31.67 203 210
u^3 P40^3 225 200 1 P2O GF4
upper limit 8 1 VV2 VV7 algebraic
s VIM
AM
DOB 7.983 lower limit .005 GF3 loop
256 0.01028 1 188
264 61 breaking 186
VV1 GF3 220 189
266 P4O DVS 248 251 62 197 AHM AH4 6
5 1 211
MO2 241 216 AHC
1 1 s xo 1 0.0785 185
VIM
8.0001 RMO 8.0001 1 0.1 0.9996
265 2400 232 AH2 187 AH1
57.14 0.301 1
224 OSA
60 6 s
271 234 215 AHM 10u
u^3 POT ^3 HM 255 APD
xo 1 VVE 202 GP3
271 P3O 196
1 242 250 0.5 158A
PVO 244 221 NOD
s BFN 1 CNZ 183
OVA upper limit 15.0
40 1 AM 6 1 176 182
223 P3O^3 u^3 lower limit 0.4 175
272 233 POM AAR RFN AHM 0.3333
upper limit 8 CNY NOD
QO2 200 CNA CN8
POT 1.5 142 0.14
P1O 0.00333 0.08 1.2 0.1024 AH
PM5 PDO 195 ARF 184
243 0.3 201 207 213 214 222 lower limit 3
122 CNR
2.8 PMO 249 1
0.5 1.2
2.859 8 139
8 512 EXC lower limit 0
VPF 40
HM RFN RBF 0.001 177 178
POT 1 0.025 2.5
0.0125 PRA 179 180 AHY
PVO lower limit 0.35 RBF 1.2 0
40 CNX AHZ
8
1
RFN AH7 s
AUM 100
0.9999 1.2 1 AHM CNE
AOM 0.0007
10 2
REK 181
1 1 28 AM
0.9864 PPC 1 AU AH8
AMM
1

1
lower_limit_0
1
NON-MUSCLE LOCAL BLOOD FLOW CONTROL 40
POV
POB
278 277 276 275 274 POD 273
ARM
1 ANM 40
algebraic
loop 2.9 CAPILLARY MEMBRANE DYNAMICS ANTIDIURECTIC HORMONE CONTROL
1 breaking RVS
0.9387 AVE
1 lower limit 0.95 66
42 41A DP0
s AK1 lower limit 0.2 POK 1 1 79
xo 1 ARM 1.6379 0.007
POR 38 s xo 0 PPD
1 0.06 36 CN7 PVG
1 40 1 1 ANU 1.79 BFN 0
AR1 43 RV1 67 DPL
0.0212 0.2
AMM 2.8 78
290 3.7 PVS 77
VIM RVS 41 39 DLP
RAM RSM RV1 CN2 85
96.3 0.04
17 17 PC LPK
AUM CPR DPP 162
POA 279 35 RAM ANM 1 163
281 280 1.6 ANU 1 2.9 17 0.00047
285 282 ARM 3 AN5 3.3
AR3 VB
AR1 37 BFM PC 5 PC
VIM PGS 5.002
1 VIM 1 RAR 2.781 16.79 1.004 160
A2K 80 lower limit 0.7 AN3 161
s lower limit 0.5 PON 30.5 17 70
xo 1 AUM PAM VB 68
PAM 1.011 RVS 61 PRP AN2 0.042
20 RAR VRC 62 CPP 1 ANM 4.0 10u
1 0.1 1.2
AR2 VVE s xo
34 BFM 2 210
AUM AUM
VV7 72 VP REK
100 RBF 0.3216 VP 159
0 CFC
1 4 69 PPC 153b
PIF 0.007 28 0.4 153a 1
284 PA BFN QAO PVS
CPP 1.2 RFN s xo
-6.3 (1.2/u)^3 ANC 1
POC 283 100 5 6 VVR 3.774 16.79
287 286 POJ 2.859 69.76
284b 0.495 0.00355 VBD DVS 2.95 (1.2/RFN)^3
VTC 10
31 7 8 9 CNE
2 1 VVS VV8 PTC 73 PPC 10
33 RSN 0.002 74 CPP
0.33 1 s 154 155 156 157 158
288 11520 32 BFN PVS
lower limit 0.3 PA PGS 3.25 xo 5 CNA CNE
1 VAS VAE u^3 142 AN1
A3K 0.3 if (POD<0) {POJ=PODx3.3} 0.3 VVE lower limit 0.0001 75 ANM
s QVO 0.0825
1 0.85 xo 2.8 VVS 3.7 0.001879 CP1
POZ VTC PC^3
289 100 QVO CV
74
PVS 1.6283e-007
AR3 VAS3 152 0.1 15
1 CPK
s DAS CPI ANT
1 xo 60
TVD DPC
0.001 70 0.04
VAS VVS 71
PA 0.001 VPD
VUD VP
59 VB 1 0.03824
5
29 HSL
LVM
1
1.4 58 VLA
5 DFP
3 xo s ANGIOTENSIN CONTROL
30 3 20
QAO VPA VRA DPC
QLN
0
HMD LVM PA2 3.002
VTL
QLO PVS
HPL
PLA 0.002 VP
5.07 45 10
QLO 46 QLO
0.01453 PR1
291 POT 0
292 POQ 1 0.6 PVS 0.9984 20.039
PLA 0 260 173
QLN AM 174 172
8 LVM = f(PA2) QRF
1 AM AM5 19.8
8 upper limit 8 10u
PA 44
lower limit 4
0 1 ANM AM2
100 RVG
27 47 AM3
28 2.738 164 171
294 POQ 8 15
4
3 293 P2O 0.1 VLE 1
CPA
RVM 1 -0.017
295 11 167 168
296 8 0.4 PLA 54 PA
298 297 53 49 AMP AM1
QLN 100
EXE 26
48 AUH
VLA sqrt HSR
1.24 25 0.03791
EXC RPA QVO 0.001879 DPL
0 50 1
Z12 QLO 20 107 AMT 169
1 -4 HPR AMR
PP1 1.4 0
1 QLN = f(PLA) VTL VTL PLD 0 200 60
VLA 1
AUC CALCULATION s 106 AMP = f(PA)
56 HMD HMD 0.004
1 55 PIF 0.00352
12 5.045 165 166
AUC xo 7.8
PA1 when PA1<40: AUC=1.2 RVM QRO 0.002 lower limit 5
PA1 AUC RPV CKE KN1 1
when 40>PA1<80: AUC=0.03*(80-PA1) 20.18 5
lower limit 0 PTC 108 s
when PA1>=80: AUC=0 170
xo
307 DPL AMC
1 0.4 0.0357 16 DRA 5 CPI
302 303 20 52 15 CNA lower limit 6
0.1 142
AUC calculation AU6 DLA 0 PTC
57 PP2 0 50 13 0.04 9 1
24 PL1 105
PLA 1
A1B 301 RVM = f(PP2) xo 109
DAU CPI
51 QRN PRA -6.334
RPT 0.026 AUH PTT
AUK AU2

AUB CALCULATION
u^3 AUB^3
0.0005
304
308
PPA VRA
1
s PIF
20 ALDOSTERONE CONTROL
305 AUH PR1
0.25 104
AUB 0
when PA1<40: AUB=1.85718 1 20 lower limit 4
PA1 AUB -4 DPC GP1
when 40>PA1<170: AUB=0.014286*(170-PA1) 1 0.04
s QRN = f(PRA) VRA
when PA1>=170: AUB=0 QPO 102 103
xo PPA DPI IFP
Z8 19 18 15 VIF
15.18 1
309 23 PLA 20 QRO 14 DPL
AUB calculation 0 6 PRA 0.005 s
RPT 12 xo 8.154e-006
22 21 PRA
QPO VPE VPA 1 0.1 110
AU8 PGL PPA s
0.09477 GPD VID 0
xo 0.38 0
AUZ CKI 133 CCD 134 135
0.30625 VTL
AUN CALCULATION 15 GP2 VID
VPA 132
1 0.0048 VIC
310 1
when PA1<50: AUN=6 AUN 111
PA1 AUN 1 0.002 0.0005 0.01 s
311 CNA 25 xo
when 20>PA1<50: AUN=0.2*(50-PA1) 83
AUJ 1 VTC 87
when PA1>=50: AUC=0 AU VIC
u
v s xo 1 CIRCULATORY DYNAMICS VID
20
0 PIF
AUN calculation GPD 131
AUJ^AUZ
316 VTD 12 VIF PTS -6.3 KI
317 0.21 0.9993 VV9 171
AUM AU9 84 xo 112 1
AUV 312 AUL 3.159 s
0.85 AU 1 xo
314 xo 128
1 313 VVR s 130 129
0.3 88 1 KIR
PLA 0 KCD KIE
0.15 s 3550 2850
0.999 0 10
AUD 2.95 0 8 POT VIM
12 PTS = f(VIF)
0.7 VVR 70 KE1
150 329 339 VIM 86 GPR 127
2.949 PPA PO1 0.013
315 0.4667 CPN 1 VTS CKE
CPP
8.25 VG
136 28 VG 5
0.9998 15 146 8
AUH AUH PPR PO2 338 11.98 113
1 149 100 15 101 140
PPC PA AM
1 AUY 1 VPF 0.333 1
319 1.5 VTS
320 0.9994 0.55 137 PPA KCD
318 0.5 1 0.4 151 HSR 85 1 0.00014
AUM lower limit 0.2375 HSL POT 121 122
0.000225 s 100 15 s 5
VIE 337 1 350 xo KED 123 124
xo 1 0.0028 KE CKE
1 POY PTT = (VTS/12)^2 (u/12)^2 1
AVE 138 147 340 345
0.9997 6 KID 75 xo s
AVE
0.375 464e-7 PTT 11.4
PPD 330
-9.648e-008 97
148 125
PPN
AUTONOMIC CONTROL PPD POS
0.5333
341
PPA4
346
PP3
351
0.0025
100
VGD 0.013332
120 126
PCP 0 RC1 HM2 0.00042
u^0.62 5 PP3^0.1 KOD
u^0.625 PA4^0.62 5
336 98
PPC 331 HMK HPL DHM 96
PLF 1 V2D REK
POS 90 1
139 352
0.07026
SVO PLF 145 0.0003 HPR 0.1 u^2 CHY^2 117 CNA
PPI 152 RCD 2 336b xo 118
32 322 347 NOD
342 1 1 NED 119
SVO 327 323 332 CNA 142.1
328 2 PPO xo s 93 1 NAE
HR 94 95 PG2
CPF 1 PGC 0.25 xo s
0 0.4 PGR 99 2130
PRA 144 s 0.1
0.0003
140 116
HM
QLO 11 PIF 142
321 2 57600
324 335 HM 57600 348 upper limit 1
326 325 343 PGP
40 40 NID
VRC PTC
HMD PFI PGH STH 0.1
1 PPI 40 HMD
AU 1
5 143 0.0000058 VIC
PTS PIF
0.5 1 141 DFP 1 VG 89 VPF 114 115
PLF 333 RKC 90 91 92 0.0125
1 1 2-(0.15/u) PPI = 2 - (0.15/VPF) VEC
-1.154e-008 334 39.97
100 344 349 1 57 CHY
VB PRM VTW
DFP HYL VTW
VPF 5 HMD -5.9 3 VP
142 0.01252 VRC
VPF VRC 1 1
1 RC2 24.2
HEART RATE AND STROKE VOLUME 0
0.0125 xo s 2
1 xo s
HPL
1 1 xo s
HPR
1
12
VTS
0.0125

PULMONARY DYNAMICS AND FLUIDS RED CELLS AND VISCOSITY HEART HYPERTROPHY OR DETERIORATION TISSUE FLUIDS, PRESSURES AND GEL ELECTROLYTES AND CELL WATER

LIST OF VARIABLES AUK-time constant of baroreceptor adaptation DLP-rate of formation of plasma protein by liver [g/min] KID-rate of potassium intake [mmol/min] PLD-pressure gradient to cause lymphatic flow [torr] QLN-basic left ventricular output [l/min] STH-effect of tissue hypoxia on salt and water intake
AUL-sensitivity of sympathetic control of vascular capacitance DOB-rate of oxygen delivery to non-muscle cells [ml O2/min] KOD-rate of renal loss of potassium [mmol/min] PLF-pulmonary lymphatic flow [torr] QLO-output of left ventricle [l/min] SVO-stroke volume output [l]
AUM-sympathetic vasoconstrictor effect on arteries DPA-rate of increase in pulmonary volume [l/min] LVM-effect of aortic pressure on left ventricular output PMO-muscle cell PO2 [torr] QOM-total volume of oxygen in muscle cells [ml] TRR-tubular reabsorption rate [l/min]
AUN-effect of CNS ischemic reflex on auto-regulation DPC-rate of loss of plasma proteins through systemic capillaries [g/min] MMO-rate of oxygen utilization by muscle cells [ml/min] POD-non-muscle venous PO2 minus normal value [torr] QO2-non-muscle total cellular oxygen [ml] TVD-rate of drinking [l/min]
AUV-sensitivity control of autonomies on heart function DPI-rate of change of protein in free interstitial fluid [g/min] M02--rate of oxygen utilization by non-muscle cells [ml/min] POK-sensitivity of rapid system of autoregulation QPO-rate of blood flow into pulmonary veins and left atrium [l/min] VAS-volume in systemic arteries [l]
AAR-afferent arteriolar resistance [torr/l/min] AUY-sensitivity of sympathetic control of veins DPL-rate of systemic lymphatic return of protein [g/min] NAE-total extracellular sodium [mmol] PON-sensitivity of intermediate autoregulation QRF-feedback effect of left ventricular function on right ventricular function VB-blood volume [l]
AHM-antidiuretic hormone multiplier, ratio of normal effect AUZ-overall sensitivity of autonomic control DPO -rate of loss of plasma protein [g/min] NED-rate of change of sodium in intracellular fluids [mmol/min] POS-pulmonary interstitial fluid colloid osmotic pressure [torr] QRN-basic right ventricular output [l/min] VEC-extracellular fluid volume [l]
AM-aldosterone multiplier, ratio of normal effect AVE-sympathetic vasoconstrictor effect on veins DRA-rate of increase in right atrial volume [l/min] NID-rate of sodium intake [mmol/min] POT-non-muscle cell PO2 [torr] QRO-actual right ventricular output [l/min] VG-volume of interstitial fluid gel [l]
AMC-aldosterone concentration AlK-time constant of rapid autoregulation DVS-rate of increase in venous vascular volume [l/min] NOD-rate of renal excretion of sodium [mmol/min] POV-non-muscle venous PO2 [torr] QVO-rate of blood flow from veins into right atrium [l/min] VGD-rate of change of tissue gel volumes [l/min]
AMM-muscle vascular constriction caused by local tissue control, ratio to resting state A2K-time constant of intermediate autoregulation EVR-postglomerular resistance [torr/l] OMM-muscle oxygen utilization at rest [ml/min] POY-sensitivity of red cell production RAM-basic vascular resistance of muscles [torr/l/min] VIB-blood viscosity, ratio to that of water
AMP-effect of arterial pressure on rate of aldosterone secretion A3K-time constant of long-term autoregulation EXC-exercise activity, ratio to activity at rest OSA-aortic oxygen saturation POZ-sensitivity of long-term autoregulation RAR-basic resistance of non-muscular and non-renal arteries [torr/l/min] VIC-cell volume [l]
AMR-effect of sodium to potassium ratio on aldosterone secretion rate A4K-time constant for muscle local vascular response to metabolic activity EXE-exercise effect on autonomic stimulation OSV-non-muscle venous oxygen saturation PO2-oxygen deficit factor causing red cell production RBF-renal blood flow [l/min] VID-rate of fluid transfer between interstitial fluid and cells [l/min]
AMT-time constant of aldosterone accumulation and destruction BFM-muscle blood flow [l/min] GFN-glomerular filtration rate of undamaged kidney [l/min] OVA-oxygen volume in aortic blood [ml O2/l blood] PPA-pulmonary arterial pressure [torr] RC1-red cell production rate [l/min] VIE-portion of blood viscosity caused by red blood cells
ANC-angiotensin concentration BFN-blood flow in non-muscle, non-renal tissues [l/min] GFR-glomerular filtration rate [l/min] OVS-muscle venous oxygen saturation PPC-plasma colloid osmotic pressure [torr] RC2-red cell destruction rate [l/min] VIF-volume of free interstitial fluid [l]
ANM-angiotensin multiplier effect on vascular resistance, ratio to normal CA-capacitance of systemic arteries [l/torr] GLP-glomerular pressure [torr] O2M-basic oxygen utilization in non-muscle body tissues [ml/min] PPD-rate of change of protein in pulmonary fluids RCD-rate of change of red cell mass [l/min] VIM-blood viscosity (ratio to normal blood)
ANN-effect of sodium concentration on rate of angiotensin formation CCD-concentration gradient across cell membrane [mmol/l] GPD-rate of increase of protein in gel [l/min] PA-aortic pressure [torr] PPI-pulmonary interstitial fluid pressure [torr] REK-percent of normal renal function VLA-volume in left atrium [l]
ANP-effect of renal blood flow on angiotensin formation CHY-concentration of hyaluronic acid in tissue fluids [g/l] GPR-total protein in gel [g] PAM-effect of arterial pressure in distending arteries, ratio to normal PPN-rate of pulmonary capillary protein loss [g/min] RFN-renal blood flow if kidney is not damaged [l/min] VP-plasma volume [l]
ANT-time constant of angiotensin accumulation and destruction CKE-extracellular potassium concentration [mmol/l] HM-hematocrit [%] PC-capillary pressure [torr] PPO-pulmonary lymph protein flow [g/min] RKC-rate factor for red cell destruction VPA-volume in pulmonary arteries [l]
ANU-nonrenal effect of angiotensin CKI-intracellular potassium concentration [mmol/l] HMD-cardiac depressant effect of hypoxia PCD-net pressure gradient across capillary membrane [torr] PPR-total protein in pulmonary fluids [g] RM0-rate of oxygen transport to muscle cells [ml/min] VPD-rate of change of plasma volume [l]
AOM-autonomic effect on tissue oxygen utilization CNA-extracellular sodium concentration [mmol/l] HPL-hypertrophy effect on left ventricle POP-pulmonary capillary pressure [torr] PRA-right atrial pressure [torr] RPA-pulmonary arterial resistance [torr/l/min] VPF-pulmonary free fluid volume [l]
APD-afferent arteriolar pressure drop [torr] CNE-sodium concentration abnormality causing third factor effect [mmo/l] HPR-hypertrophy effect on heart, ratio to normal PDO-difference between muscle venous oxygen PO2 and normal venous oxygen PO2 [torr] PRM-pressure caused by compression of interstitial fluid gel reticulum [torr] RPT-pulmonary vascular resistance [torr/l/min] VRA-right atrial volume [l]
ARF-intensity of sympathetic effects on renal function CPG-concentration of protein in tissue gel [g/l] HR-heart rate [beats/min] PFI-rate of transfer of fluid across pulmonary capillaries [l/min] PRP-total plasma protein [g] RPV-pulmonary venous resistance [torr/l/min] VTC-rate of fluid transfer across systemic capillary membranes [l/min]
ARM-vasoconstrictor effect of all types of autoregulation CPI-concentration of protein in free interstitial fluid [g/l] HSL-basic left ventricular strength PFL-renal filtration pressure [torr] PTC-interstitial fluid colloid osmotic pressure [torr] RR-renal resistance [torr/l/min] VTD-rate of volume change in total interstitial fluid [l/min]
AR1-vasoconstrictor effect of rapid autoregulation CPN-concentration of protein in pulmonary fluids [g/l] HSR-basic strength of right ventricle PGC-colloid osmotic pressure of tissue gel [torr] PTS-solid tissue pressure [torr] RSM-vascular resistance in muscles [torr/l] VTL-rate of systemic lymph flow [l/min]
AR2-vasoconstrictor effects of intermediate autoregulation CPP-plasma protein concentration [g/l] HYL-quantity of hyaluronic acid in tissues [g] PGH-absorbency effect of gel caused by recoil of gel reticulum [torr] PTT-total tissue pressure [torr] RSN-vascular resistance in non-muscle, n/minon-renal tissues [torr/l/min] VTW-total body water [l]
AR3-vasoconstrictor effect of long-term autoregulation CV-venous capacitance [l/torr] IFP-interstitial fluid protein [g] PGL-pressure gradient in lungs [torr] PGV-pressure from veins to right atrium [torr] RVG-resistance from veins to right atrium [torr/l/min] VUD-rate of urinary output [l/min]
AU-overall activity of autonomic system, ratio to normal DAS-rate of volume increase of systemic arteries [l/min] KCD-rate of change of potassium concentration [mmol/min] PGP-colloid osmotic pressure of tissue gel caused by entrapped protein [torr] PVG-venous pressure gradient [torr] RVM-depressing effect on right ventricle of pulmonary arterial pressure VV7-increased vascular volume caused by stress relaxation [l]
AUB-effect of baroreceptors on autoregulation DFP-rate of increase in pulmonary free fluid [l/min] KE-total extracellular fluid potassium [mmol] PGR-colloid osmotic pressure of interstitial gel caused by Donnan equilibrium [torr] PVO-muscle venous PO2 [torr] RVS-venous resistance [torr/l/min] VVR-diminished vascular volume caused by sympathetic stimulation [l]
AUC-effect of chemoreceptors on autonomic stimulation DHM-rate of cardiac deterioration caused by hypoxia KED-rate of change of extracellular fluid potassium concentration [mmol/min] PIF-interstitial fluid pressure [torr] PVS-average venous pressure [torr] SR-intensity factor for stress relaxation VVS-venous vascular volume [l]
AUH-autonomic stimulation of heart, ratio to normal DLA-rate of volume increase in pulmonary veins and left atrium [l/min] KI-total intracellular potassium concentration [mmol/l] PLA-left atrial pressure [torr] QAO-blood flow in the systemic arterial system [l/min] SRK-time constant for stress relaxation Z8-time constant of autonomic response

Figure 8: Guyton's overall regulation model of Circulation - implementation in Matlab/Simulink. The layout
and block numbering is exactly the same as in the original Guyton's scheme (Fig. 2). The difference is, that
this scheme is also a fully functional simulation model.

10
 ISBN 987-80-7080-658-6, CD ROM Proceedings, http://www.humusoft.cz/akce/matlab07

NON-MUSCLE OXYGEN DELIVERY MUSCLE BLOOD FLOW CONTROL AND PO2

0.01251
39.96 198.5

VPF OVA
HM 8.005 0.0125
40 200
VPF MUSCLE BLOOD FLOW CONTROL AND PO2
HM 39.96 OVA
INTPUTS:
POT VPF - volume of free fluid in the pulmonary interstitium
HM 8
198.5 8 HM - hematocrit [%]
NON-MUSCLE OXYGEN DELIVERY 40
BFM - blood flow in muscles
POT P2O
HM [l/min]
OVA INTPUTS:
200 1.019 EXC - Effect of excercise on the metabolic usage 8
HM-hematocrit [%] of oxygen by the muscles [ratio to resting state]
OVA OVA-oxygen volume in aortic blood [ml O2/l blood] P2O
AU - overall activity of autonomic system
BFN-blood flow in non-muscle, non-renal tissues [l/min] BFM
1
AOM-autonomic effect on tissue oxygen utilization OUTPUTS: 0.9982
2.857 BFM OVA - oxygen content of arterial blood
OUTPUTS: [ml O2 STPD/l blood] AOM
BFN POT-non-muscle cell PO2 [torr] 40 P2O -
2.8 POV-non-muscle venous PO2 [torr] 1
1 EXC AOM - autonomic effect on tissue oxygenation
BFN AMM - muscle vascular constriction caused by logical tissue control AOM
EXC [multiplifier, ratio to normal]
0.9982 POV 0.9879 0.9996
40
AU AMM
POV
AOM 1 1
1
AU
AOM AMM
Muscle Blood Flow Control And pO2

NON-MUSCLE OXYGEN DELIVERY

THIRST AND DRINKING

NON-MUSCLE OXYGEN DELIVERY MUSCLE BLOOD FLOW CONTROL AND PO2 KIDNEY DYNAMICS AND EXCRETION
100 7.999 1.005
0.01251
39.99 198.7 THIRST AND DRINKING
PA
100 0.0009778 POT STH
VPF 8 INTPUT:
HM 0.0125 OVA 1
POT - non muscle cells PO2 [torr]
40 7.999
VPF MUSCLE BLOOD FLOW CONTROL AND PO2 200 VASCULAR STRESS RELAXATION PA
27.99 VUD
POT AHM - antidiurectical hormone effect to non renal
STH
HM 39.99 vascular resistance, multiplifier
OVA
INTPUTS: 0.001 (ratio to normal effect)
POT VPF - volume of free fluid in the pulmonary interstitium PPC 0.9995 OUTPUT:
HM 7.982 28 VUD
198.7 8 HM - hematocrit [%] KIDNEY DYNAMICS AND EXCRETION STH - salt appetite multiplifier factor 0.001
NON-MUSCLE OXYGEN DELIVERY 40
BFM - blood flow in muscles VASCULAR STRESS RELAXATION PPC [ratio to normal]
POT P2O 0.3219 INTPUTS:
HM [l/min] 0.01041 TVD - rate of intake of fluid by mouth
OVA INTPUTS: 0.9988 PA - aortic pressure [torr] AHM TVD
200 1.013 EXC - Effect of excercise on the metabolic usage 8 INTPUT: 1 or otherwise [l/min]
HM-hematocrit [%] of oxygen by the muscles [ratio to resting state] VVE - VVE - excess blood (stressed) volume in the veins [l] PPC - plasma colloid osmotic pressure [torr] 0
OVA OVA-oxygen volume in aortic blood [ml O2/l blood] P2O VIM VIM - blood viscosity (ratio to normal blood AHM
AU - overall activity of autonomic system VVE VV7
BFM 0.3 1 TVD
BFN-blood flow in non-muscle, non-renal tissues [l/min] 1 0 [torr min/ll] 1.201
AOM-autonomic effect on tissue oxygen utilization OUTPUTS: 1 OUTPUT: VIM REK - percent of normal renal function [ratio to normal]
2.861 BFM OVA - oxygen content of arterial blood VV7 - increased vascular volume caused by stress relaxation [l] CNE - sodium concentration abnormability RBF Thirst And Drinking
OUTPUTS: [ml O2 STPD/l blood] AOM causing third factor effect [mmol/l]
POT-non-muscle cell PO2 [torr] AUM - sympathetic vasoconstrictor effect 1.2
BFN 40 P2O -
2.8 POV-non-muscle venous PO2 [torr] 1 1 REK on arteries [ratio of normal effect]
1 EXC AOM - autonomic effect on tissue oxygenation
RBF
BFN AMM - muscle vascular constriction caused by logical tissue control AOM AHM - antidiuretic hormone [ratio of normal effect]
EXC Vascular Stress Relaxation REK
[multiplifier, ratio to normal] AM - aldosterone multiplier [ratio of normal effect]

1 POV 1.003 0.9873 9.834

40 OUTPUTS:
AU AMM CNE VUD - rate of urinary output [l/min]
POV
AOM 1 1 10 RBF- renal blood flow [l/min] 1.201
1 RFN - renal blood flow if kidney is not damaged [l/min]
AU CNE
AOM AMM NOD - rate of renal excretion of sodium [mmol/min] RFN
Muscle Blood Flow Control And pO2 1.002 1.2
AAR - afferent arteriolar resistance [torr min/l]
NON-MUSCLE OXYGEN DELIVERY AUM EVR - postglomerular resistance [torr min/l] RFN
1 RR - renal resistance [torr min/l]
AUM GLP - glomerular pressure [torr]
GFN - glomerular filtration rate of undamaged kidney [l/min] ANGIOTENSIN CONTROL
0.9995 GFR - glomerular filtration rate [l/min]

AHM 1.003
1 0.09917
AHM NOD AU
0.9925 0.1 1
ANTIDIURECTIC HORMONE CONTROL
NOD AU
AM
1 INTPUT:
0.09827 0.9995
AU - overall activity of autonomic system,
AM ratio to normal
Kidney Dynamics and Excretion PRA - right artial pressure
PRA AHM
0 CNA - extracellural sodium contrentration
1
PRA OUTPUT:
AHM
AHM - antidiurectic hormone multiplifier,
142.2 ratio of normal effect

CNA
142
NON-MUSCLE LOCAL CNA
BLOOD FLOW CONTROL Antidiurectic Hormone Control
CIRCULATORY DYNAMICS
NON MUSCLE LOCAL BLOOD FLOW CONTROL 0.9399

INTPUT:
40 POT - non-muscle cells PO2 [torr] ARM 1.013
0.9399 1.6
POV ARM
OUTPUT:
ARM BFM
ARM - vasoconstrictor effect of local blood flow 0.9988
40 autoregulation in non-muscle tissues 1
1
[ratio to normal]
POV VIM BFM
ARM 1 ANGIOTENSIN CONTROL
VIM
Non-Muscle Local Blood Flow Control 1.002
2.784
AUM
1 RVS
2.9
AUM 0.9985
0.9985
RVS CAPILLARY MEMBRANE DYNAMICS REK
1 REK

ANGIOTENSIN CONTROL ANM

ANM
1 0.0009778 1
INTPUTS:
ANM 3.775 1.201 REK - percent of normal renal function ANM
0.9873 16.82
VUD [ratio to normal]
PVS 0.001 RFN - renal blood flow if kidney is not damaged [l/min]
AMM PC CNA - extracellural sodium concentration
3.7 VUD RFN
1 2.784 1.2
17
AMM PVS
1.001 PC RFN OUTPUTS:
RVS
2.9 ANM - angiotensin multilier factor on vascular resistance 9.834
[ratio to normal]
AVE 0.3219 RVS
1 2.861 142.2 CNE - sodium concentration abnormality causing third factor effect
CIRCULATORY DYNAMICS CNE
AVE
1.201 VVE 5.001 10
INTPUTS: BFN CNA
ARM - vasoconstrictor effect of all types of autoregulation 0.3 2.8 142 CNE
VIM - blood viscosity (ratio to normal blood) VB
RBF VVE BFN CNA
1.2 AUM - sympathetic vasoconstrictor effect on arteries 3.775 5
ANM - angiotensin multiplier effect on vascular resistance, ratio to normal VB
RBF
16.82 AMM - muscle vascular constriction caused by local tissue control, ratio to resting state
PVS Angiotensin Control
AVE - sympathetic vasoconstrictor effect on veins 0.09827 3.7
RBF - renal blood flow [l/min]
AUTONOMIC CONTROL 17
PC PC - capillary pressure [torr]
PRA
PVS 2
CAPILLARY MEMBRANE DYNAMICS
VVR - diminished vascular volume caused by sympathetic stimulation [l] 3.001
PC
2.948 VV7 - increased vascular volume caused by stress relaxation [l] 0
AUH - autonomic stimulation of heart, ratio to normal VRC INTPUTS:
HMD - cardiac depressant effect of hypoxia PRA 2 PTC - colloid osmotic pressure of the tissue gel [torr] VP
1.003 VTL - rate of return of fluid from the interstitium to the
VVR HPL - hypertrophy effect on left ventricle VRC 3
100 2.95 -6.334 blood through the lymph [l/min]
VB - blood volume [l]
AU VVR TVD - rate of intake of fluid by mounth or otherwise [l/min] VP
5.075
0.01041 RVS - venous resistance
PA 1 PIF BFN - blood flow in non-muscle, non renal tissues
100 OUTPUTS: -6.3
AU BFM - muscle blood flow [l/min] QLO PVS - average venous pressure
VV7 PIF VRC - volume of red blood cell
PA 0 RVS - venous resistance [torr/l/min] 5 5.101
VUD - rate of urinary output 0.03842
PVS - average venous pressure [torr]
VV7 QLO DFP - rate of increase in pulmonary free field
1.001 VVE - excess blood (stressed) volume in the systemic veins [l]
2.948 PTC PIF - intersticial fluid pressure DPC
PRA - right atrial pressure [torr] 5
AUTONOMIC CONTROL PPD - rate od change of protein in pulmonary fluids
QLO - output of left ventricle [l/min] 0.04
AUH 100 CPI - concentration of protein in free intersticial fluid
VVR PA - aortic pressure [torr] PTC
INTPUTS: 1 -3.722e-007 VP - plasma volume [l] DPC
7.999 BFN - blood flow in non-muscle, non-renal tissues [l/min]
PA - systemic arterial pressure torr 2.95 DPL - rate of systemic lymphatic return of protela
AUH PRA - right atrial pressure [torr]
POT - non-muscle cell PO2 [torr] 1 PA
VVR PLA - left atrial pressure [torr] DFP
POT P20 - 0 OUTPUTS:
8 EXC - Effect of excercise on the metabolic usage of oxygen
by the muscles [ratio to resting state]
HMD
100
DFP
PC - systemic capillary pressure [torr]
69.97
ALDOSTERONE CONTROL
POT 1 PA 0.001 PPC - plasma colloid osmotic pressure [torr]
1.001
AUZ - overall sensitivity of autonomic control [ratio to normal] VTC - toral rate of movement of fluid out of systemic capillaries[l/min]
HMD VB - blood volume CPP
1 0.9985
OUTPUTs: 2.861 TVD CPP - plasma protein concentration
AUH 0.001 70
AU - overall activity af autonomic system DPC - rate of loss of plasma protein through systemic capillaries
[ratio to normal] 1 HPL TVD CPP
1 0.001887 ANM
AUH - autonomic multilier effect on the heart output BFN 1
7.982 AUH
[ratio to normal] HPL
5.001 2.8 ANM
VVR - basic volume of venous tree(maximum volume VTL
P2O at zero pressure) [l] BFN 0.002
8 1.002 27.99 100
AUM - autonomic multipllier effect on arterial resistance VB VTL
5 ALDOSTERONE CONTROL
[ratio to normal] -1.524e-006
P2O
AVE - autonomic multipllier effect on venous resistance VB PPC
AUM 15.19 PA INTPUT:
[ratio to normal] 100
1 PPD 28 ANM - angiotensin multiplier effect on vascular resistance,
0 0.9925
PA ratio to normal
AUM PPA PPC
1 HSR PPD PA - aortic pressure [torr]
15 20.4 CKE - extracellural potassium concentration AM
HSR 5.001
CNA - extracellural sodium concentration 1
1.001 PPA
CPI AM
20 0.001902 CKE OUTPUT:
1 EXC 5 AM - aldosterone multiplier, ratio of normal effect
1 HSL CPI
EXC AVE 0.01395 0.0385 CKE
HSL VTC
1
1 0.002 142.2
AVE PLA DPL
0.04 VTC
0
HPR DPL CNA
Autonomic Control 1
PLA 142
Capillary Membrane Dynamics
HPR
CNA
Circulatory Dynamics
Aldosterone Control

TISSUE FLUIDS, PRESSURES AND GEL ELECTROLYTES AND CELL WATER

HEART HYPERTROPHY OR DETERIORATION 0.001887 0.9925

PULMONARY DYNAMICS AND FLUIDS VTL

1
AM
7.527e-006

0.001902 0.002
100 AM VID
VTL
HEART RATE AND STROKE VOLUME 15.19
RED CELLS AND VISCOSITY 0.002
VTC
0.0385
0
PA VID
100 1
VTC 1 REK
1.003 -3.722e-007
PPA PA HPR DPL
15 REK
DFP 0.9988 1 0.04
15.19 0.09917
PPA 7.999 ELECTROLYTES AND CELL WATER
AU 0 HPR 5.001
DPL
1 VIM
DFP TISSUE FLUIDS, PRESSURES AND GEL INTPUTS:
AU 1 PPA NOD
0.01395 POT 15 5.101 0.1 AM - aldosterone multiplier, ratio of normal effect CKE
PULMONARY DYNAMICS AND FLUIDS HEART HYPERTROPHY OR DETERIORATION
8 RED CELLS AND VISCOSITY VIM REK - percent of normal renal function
INTPUTS: 5
1 PPA NOD [ratio to normal]
HEART RATE AND STROKE VOLUME INTPUTS: POT INTPUTS: VTC - rate of fluid transfer across systemic intersticial fluid PTC
PLA INTPUT: 0.04 1.005 NOD - rate of excretion of sodium in the urine [mmol/min] CKE
0 PPA - pulmonary arterial pressure [torr] 2 PA - systemic arterial pressure [torr] DPC -rate of influx protein into the interstitial fluid from plasma [g/min] 5
POT - non-muscle cell PO2 [torr] STH - salt appetite multiplier factor [ratio to normal]
INTPUTS: PLA - left atrial pressure [torr] 0.01251 PPA - pulmonary arterial pressure [torr] 1 VID - rate of fluid transfer between interstitial fluid and cells
HMD PLA VB - volume of blood [l] VTS - systemic interstitial fluid volume [l]
1 AUR - overall activity of autonomic system PPC - plasma colloid osmotic pressure [torr] HSL - basic strenght or left ventricle [ratio to normal] PTC STH
VRC DPC 1 VP - plasma volume [l]
[ratio to normal] CPP - plasma protein concentration POT - Non muscle cells PO2 [troo] 0.04 OUTPUTs:
HMD VPF OUTPUT: 2 HSL HPL 20.4 VPF - pulmonary interstitial fluid volume [l]
HMD - cardiac depresant effect of hypoxia, shock HSR - basic strenght or right ventricle [ratio to normal] PTC - total colloid osmotic pressure of the tissue gel] 142.2
VIM - blood viscosity [ratio to normal] DPC STH
and other factors [ratio to normal] SVO 0.07019 27.99 OUTPUTs: 0.0125 1 VTL - lymph flow rate [l/min]
5.001 HM - hematocrit [%] VRC 0.01251
0.09827 OUTPUTS: DPL - rate of return of protein to the circulatin by way of the lymph [g/min] OUTPUTS:
PRA - right atrial pressure [torr] DFP - rate of change of free fluid in the lungs [l/min] VRC - volume of red blood cells [] HPL CPI
VPF HPR - hypertrophy effect of right heart [ratio to normal] CPI - concentration pf protein in the interstitium [g/l] VID - rate of fluid transfer between interstitial fluid and cells [l/min]
QLO - output of left ventricle [l/min] VPF - volume of free fluid in the pulmonary interstitium [l/min] 39.99 20 CNA
PPC 7.999 HPL - hypertrophy effect of left heart [ratio to normal] VTS - total interstitial fluid volume [l] CKE - extracellular potassium concentration [mmol/l]
28 PPD - rate of loss of protein through the pulmonary capillary VB VPF
PRA 5 HMD - cardiac depresant effect of hypoxia, shock CPI 0.0125 CNA - extracellular sodium concentration [mmol/l] 142
0 OUTPUTS: membrane [g/min]
VTW - total body water [l]
SVO - stroke volume [l] PPC VB HM VPF CNA
PRA POT
40 8 11.96 3.001
-1.524e-006
5.075 HM POT 1 VTS
69.97
7.527e-006 VP
PPD Red Cells And Viscosity 12 3
QLO CPP 0 HMD
VTS VP
5 70 1 VID
PPD 0 11.96 39.95
QLO CPP HSR -6.334 VTW
HMD
VID
VTS VTW
Heart Rate and Stroke Volume PIF 12
Pulmonary Dynamics and Fluids
-6.3 VTS
Heart Hypertrophy or Deterioration
PIF
Electrolytes and Cell Water
Tissue Fluids, Pressures and Gel

Figure 9: Guyton's overall regulation model of Circulation - implementation in Matlab/Simulink using

Simulink subsystem blocks as "simulation chips".
Simulink implementation of the (corrected) Guyton's model made by us is available for
download from the address http://physiome.cz/Guyton to anyone interested. At the same address, our
Simulink implementation of a much complex sequel of the model from 1986 can be found too.
Further, there is also a detailed description of all mathematical relations used with their reasoning
(however, for the present time it is in the Czech language only).

6 From Simulink Diagram to Simulation Games During Physiological Teaching

We use Simulink implementation of Guyton's model as an educational tool to teach physiology
to undergraduate and postgraduate students at the Czech Technical University (ČVUT). This structure
of Simulink diagram (in a form of "simulation chips") is however, too abstract for medical students. It
is ideal, if their teaching models have the form of schematic pictures to which they are accustomed, for
example from the Atlas of Physiology [18]. Unlike the book, these pictures can be interactive, and

11
 Technical Computing Prague 2007. 15th Annual Conference Proceedings. Prague, 2007

195.5 NON MUSCLE O2 DELIVERY

OVA OSV 0.6632
INTPUTS: 14.1
HEART RATE AND STROKE VOLUME
OVA - oxygen content of arterial blood 99.85
MYOGENIC AUTOREGULATION AUR RESISTANCES IN THE PULMONARY CIRCULATION
[ml O2 STPD/l blood] 1.652
2.669 INTPUTS: AND PULMONARY VENOUS PRESSURE RPA
BFN - blood flow in non-muscle and non-renal tissues NON MUSCLE LOCAL BLOOD FLOW CONTROL PA HR 80.3 PPA
POV 37.9 AUR - autonomic stimulation of heart rate
[l/min] INTPUTS:
BFN 0.9625 17.67 [ratio to normal] INTPUTS:
HM - hematocrit [%] INTPUT: PA - systemic arterial pressure [torr] HMD
PC - capillary pressure [torr] HMD - cardiac depresant effect of hypoxia, shock PPA - pulmonary arterial pressure [torr]
AOM - autonomic effect on tissue oxygenation 7.728 POT - non-muscle cells PO2 [torr] RPV 1.43
PC MYOGTAU - time delay factor of myogenic response and other factors [ratio to normal] -0.4086 PLA - left atrial pressure [torr]
[ratio to normal]
40 POT POT ARM PRA - right atrial pressure [torr] QPO - rate of blood flow into pulmonary veins and left atrium [l/min]
O2M - basic oxygen utilisation in non-muscle cells OUTPUT: (in normal condition TENSTC= 240 min) PLA
0.809 MYOGRS QLO - output of left ventricle [l/min] 3.082
[ml O2 STPD/min] ARM - vasoconstrictor effect of local blood flow TENSGN - factor of effectiveness of myogenic response PRA
HM RPT
autoregulation in non-muscle tissues 240 MYOGTAU OUTPUTS: SVO 0.05863 OUTPUTS:
OUTPUTS: [ratio to normal]
DOB 168.2 MYOGTAU OUTPUT: HR - heart rate [beats/min] RPA - pulmonary arterial resistance [torr min/l]
1.025 OSV - non-muscle venous oxygen saturation [%]
MYOGRS - myogenic autoregulation effect on vascular resistance QLO SVO - stroke volume [l] RPV - pulmonary venous resistance [torr min/l]
POV - non muscle venous PO2 [torr] QPO 10.81
1 TENSGN in muscle and in non-renal tissue [multiplier, ratio to normal] RPT - total pulmonary vascular resistance [torr min/l] PVP
POT - non muscle cell PO2 [torr] PPA
AOM Non-muscle Local Blood Flow Control PVP - pulmonary venous pressure [torr]
DOB - rate of oxygen delivery to non-muscle cells TENSGN
MO2 168.6 Heart Rate and Stroke Volume
[ml O2 STPD/min]
Myogenic Autoregulation Resistances in the Pulmonary Circulation and Pulmonary Venous Pressure
MO2 - rate of oxygen utilisation by non-muscle tissues
[ml O2 STPD/min] 1.009
QO2 - non-muscle total cellular oxygen 2321 THE VOLUME RECEPTOR FEEDBACK MECHANISM
164.5 O2M QO2
[ml O2 STPD]
O2M
INPUTS: 0.905 OSA
PRA AH7
PRA - riight atrial pressure [torr]
Delivery of Oxygen to the Non-muscleTtissues ATRVHBM - sensitivity controller of volumereceptor feedback effect
on change of basic of venous system
[ATRVFB=AH7*ATRRVBM, no effect = 0]
0
ATRRFBM - sensitivity controller of volumereceptor feedback effect
195.5 MUSCLE O2 DELIVERY on nonmuscle arterial resistance PA
0.0118 0.9775 14.1
0.6667 [ATRRFB=AH7*ATRRFBM, no effect = 0]
OVA INTPUTS: OV S 0 ATRV FBM ATRVFB
OVA - oxygen content of arterial blood ATRVFBM OUTPUTS: 0.809
0.9915 [ml O2 STPD/l blood] AH7 - effect of right atrial volume receptor reflex on ADH 4.708
VPF BFN - blood flow in muscles secretion [relative additive factor, normal value = 0]
1 PPA
BFM [l/min] PVO 38.09 MUSCLE LOCAL BLOOD FLOW CONTROL ATRVFB - change in basic volume of venous system
168.2 HM - hematocrit [%] caused by atrial volume receptor feedback
INTPUT: PRA RIGHT HEART PUMPING
PULMONARY O2 DELIVERY 40 AOM - autonomic effect on tissue oxygenation ATRRFB - multiplier factor for the effect on muscle and
DOB [ratio to normal] 7.754 PMO - muscle cells PO2 [torr] 0 ATRRFBM ATRRFB
OSA non-renal vacular resistance of feedback from the atrial INTPUTS: LEFT HEART PUMPING
INTPUTS: OMM - basic oxygen utilisation in muscles PPA QRO PLA
HM PMO PMO AMM 0.9503 ATRRFBM stretch receptors [multiplier, ratio to resting state]
61.53 OUTPUT: PRA - right atrial pressure [torr]
VPF - volume of free fluid in the pulmonary interstitium [l/min] [ml O2 STPD/min] INTPUTS: QLO
AMM - vasoconstrictor effect of local blood flow PPA - pulmonary arterial pressure [torr] PA
DOB - non-muscle oxygen usage[ml/min] EXC - Effect of excercise on the metabolic usage AUH PA PLA - left atrial pressure [torr]
RMO 1.025 61.53 autoregulation in muscles AUH - autonomic stimulation of heart [ratio to normal] 4.708
RMO - muscle oxygen usage [ml/min] of oxygen by the muscles [ratio to resting state] The volume receptor feedback mechanism PA - systemic arterial pressure [torr]
[ratio to normal] OSA - oxygen hemoglobin saturation
PO2DEF - normalised difussion coecficient for oxygen AUH - autonomic stimulation of heart [ratio to normal]
AOM RMO OSA HSR - basic strenght or right ventricle [ratio to normal]
through the pulmonary membrane [at norma PO2DEF=1] OUTPUTS: AUH OSA - oxygen hemoglobin saturation
HPR - hypertrophy effect of heart [ratio to normal]
1 PO2DEF PO2MAB - ambient oxygen pressure [torr] OVS - muscle venous oxygen saturation [%] HSL - basic strenght or left ventricle (ratio to normal)
HSR HMD - cardiac depressant effect of hypoxia. shock 6.965
HM - hematocrit PVO - muscle venous PO2 [torr] HSR QRN HPL - hypertrophy effect of left heart [ratio to normal]
PO2DFF Muscle Local Blood Flow Control PA and other factors [ratio to normal] OSA QLN
PMO - muscle cell PO2 [torr] HMD - cardiac depressant effect of hypoxia, shock
61.5 QLO - output of left ventricle [l/min]
OUTPUTs: 60 OMM RMO - rate of oxygen delivery to muscles MMO HEART HYPERTROPHY OR DETERIORATION HPR HPR HPR and other factors [ratio to normal]
QLN - normalised output of the left heart [l/min] 4.46
150 PO2AMB OSA - arterial oxygen saturation OVA [ml O2 STPD/min] HSL
OMM HSL
PO2AMB OVA - arterial blood oxygen content [ml O2/l blood] MMO - rate of oxygen utilisation by muscles QAO INTPUTS: HMD OUTPUTS:
1.001 HMD OUTPUTS:
[ml O2 STPD/min] PA - systemic arterial pressure [torr] QLO - actual left ventricular output [l/min]
QRO - actual right ventricular output [l/min]
1 EXC QOM - muscle total cellular oxygen QOM 2397 QAO - blood flow in the systemic arteriel system [l/min] HPL QLN - normalised lwft ventricular output [l/min]
HM QRN - normalised right ventricular output [l/min] 1.012 1.005
[ml O2 STPPD] PPA PPA - pulmonary arterial pressure [torr] QLO RVM LVM - depressing effect on left ventricle of pulmonary LVM
EXC RVM - depressing effect on right ventricle of pulmonary
HSR - basic strenght or right ventricle [ratio to normal] arterial pressure [ratio to normal]
1 arterial pressure [ratio to normal] HMD
Pulmonary O2 Delivery HSL - basic strenght or left ventricle [ratio to normal] HPL QLN
40 Delivery of Oxygen to the Muscles POT - Non muscle cells PO2 [troo]
0.1 HSR
Right Heart Pumping Left Heart Pumping
HSR OUTPUTS:
HPR - hypertrophy effect of right heart [ratio to normal] HPL
1 HSL HPL - hypertrophy effect of left heart [ratio to normal]
HSL HMD - cardiac depresant effect of hypoxia, shock
HSL HMD
HMD
4.46
POT
1
4.708
Heart hypertrophy or deterioration
HM

99.85
2.915
DFP
V VR UNSTRESSED SYSTEMIC VENOUS VOLUME
PPA
AUTONOMIC CONTROL OF THE CIRCULATION 0.9143 99.85
VPF AU 1.167 INPUTS:
PA ANU VVR - normal maximum volume of blood PA
0.0007524 VB CIRCULATORY DYNAMICS - FLOWS AND PRESSURES
INTPUTS: 4.017
in the venous system at zero pressure [l]
PULMONARY FLUID DYNAMICS PA - systemic arterial pressure torr
PCP 0.1393 VENOUS STRESS RELAXATION ANU - nonrenal effect of angiotensin [ratio to normal] PA INPUTS: PVS
POT - non-muscle cell PO2 [torr]
AUH VV6 -0.2 ANY ANY - sensitivity of large veins to effect of angiotensin QRO VB - blood volume [l]
7.728 PMO - muscle cells PO2 [torr] 0.809
INTPUTS: INTPUTS: [normal value = -0.2 l/unit of angiotensin] QRO - actual right ventricular output l/min]
EXC - Effect of excercise on the metabolic usage of oxygen ANY V VS0 2.945 PRA
PLA PPA - pulmonary arterial pressure [torr] POT VVE - excess blood volume in the veins [l] VV6, VV7 - changes in basic volume of venous system QLO - output of left ventricle [l/min]
PLA - left atrial pressure [torr] POS 19.97 by the muscles [ratio to resting state] 1.05 QLO 14.1
V V6 cauused by stress relaxation [l] VVS0 - unstressed venous systemic vascular volume [l]
PPC - plasma colloid osmotic pressure [torr] ANUBR - direct effect of angiotensin on vasomotor center PPA
AUR VV E OUTPUTS: ATRVFB - change in basic volume of venous system VVE - excess volume (stressed volume) in systemic veins [l]
CPF - pulmonary capillary filtration coeffitient [l/min/torr] ["virtual" torr]
7.754 VV6 - increased venous vascular volume caused by atrial volume receptor feedback VVS0 VAS0 - unstressed volume in systemic arteries [l] -0.4086
-10.71 AUZ - overall sensitivity of autonomic control [ratio to normal]
PPI 1.167 caused by long time stress realaxation [l] V V7 VRA0 - unstressed right atrial volume [l] PLA
OUTPUTs: 2.915
PMO VV7 - - increased venous vascular volume OUTPUT: VPA0 - unstressed volume in pulmonary arteries [l] 0.8495
OUTPUTs: 0
DFP - rate of change of free fluid in the lungs [l/min] V VR caused by short time stress realaxation [l] VV7 VVS0 - the maximum volume ov venous system at zero volume 0.495 VAS0 VLA0 - unstressed volume in left atrium and pulmonary veins [l]
AU - overall activity af autonomic system VAS
VPF - volume of free fluid in the pulmonary interstitium [l/min] 8.891e-005 ATRVFB (so called unstressed venous volume) [l] CAS - capacitance of systemic arteries [l/torr]
PPC PFI [ratio to normal] VAS0
PCP - pulmonary capillary pressure [torr] PA CV - capacitance of venous systemic volume [l/torr]
1 AUH - autonomic multilier effect on the heart output RESISTANCES IN THE SYSTEMIC CIRCULATION 0.1 VRA0 VVS 3.277
POS - osmotic pressure in pulmonary interstitial fluid pressure [torr] CRA - capacitance of right atrium [l/torr]
PPI - pulmonary interstitial fluid pressure [torr] [ratio to normal] 1.167 Unstressed volume in systemic venous tree
AUP 35.9 VRA0 CPA - capacitance of pulmonary arteries [l/torr] 0.3314
PFI - rate of fluid filtration out of pulmonary capillary [l/min] PLF 8.664e-005 EXC AUR - autonomic multilier effect on heart rate Effect of stress relaxation on basic venous volume 0.01242 96.3 RAM INTPUTS:
0.30625 VPA0 CLA - capacitance of left atrium and pulmonary veins [l/torr] VV E
PLF - pulmonary lymph flow rate [l/min] [ratio to normal] PA - systemic arterial pressure [torr]
VVR - basic volume of venous tree(maximum volume RAM RSN - vascular resistance in non-muscle and non renal
CPN - concentration of protein in pulmonary interstitial fluid [g/l] RAM - basic vascular resistance of muscles [torr min/l] VPA0
0 30.52 RAR RSN tissues [torr min /l] VRA 0.104
PPN - protein leakage rate through the pulmonary capillary membrane [g/min] CPN 49.93 at zero pressure) [l] 1.025 1.009 RAR - basic vascular resistance of non-muscle and non-renal
AOM 0.4 VLA0 RSM - vascular resistance in muscles [torr min /l]
72 CPP PPR - total quantity of protein in pulmonary interstitial fluid [g] AUP - autonomic multipllier effect on ADH hormone excretion etc. RAR tissues [torr min/l]
[ratio to normal] VLA0 RPT -pulmonary vascular resistance [torr min /l]
CPP PPD - rate of loss of protein through the pulmonary capillary ANUBR 1.142 MYOGRSMYOGRS - myogenic autoregulation effect on vascular resistance RR - total renal resistance [torr min /l]
VPA 0.3739
membrane [g/min] AOM - autonomic multipllier effect on tissue oxygen utilisation in muscle and in non-renal tissue (multiplier, ratio to normal) 0.00355 CAS
PPN 0.004965 1.142 ( VIM - blood viscosity (ratio to normal blood)
[ratio to normal] AUM - sympathetic vasoconstrictor effect on arteries 0.3959
AUM CAS FIS - conductance fot the fistula [l/min/torr] VLA
AUM - autonomic multipllier effect on arterial resistance AUM in muscle and non-renal tissues
[ratio to normal] 0.0825 CV 4.708
1 [multiplier factor, ratio to normal]
OUTPUTS: QAO
PPR 0.5892 AVE - autonomic multipllier effect on venous resistance VIM - blood viscosity [ratio to normal] CV
AUZ VIM PA - arterial (aortic) pressure [torr]
1 [ratio to normal] 1.035 ANU - nonrenal effect of angiotensin [ratio to normal] 4.708
0.0003 CPF AVE 0.005 CRA PVS - average venous pressure [torr]
0.9143 AHM - antidiuretic hormone effect to non renal vascular QVO
AUZ PRA - right atrial pressure [torr]
CPF resistance, multiplier (ratio to normal effect) 96.65 CRA 4.708
PPD 0.0006392 ANU PPA - pulmonary arterial pressure [torr]
Autonomic Contorl of the Circulation ATRRFB - multiplier factor for the effect on muscle and 0.0048 CPA
1 PLA - left atrial mpressure [torr] QPO
non-renal vacular resistance of feedback from the atrial 2.669
CPA VAS - volume in systemic arteries [l]
Pulmonary Fluid Dynamics AHMR stretch receptors [multiplier, ratio to resting state] RSM
0.01 CLA VVS - systemic venous vascular volume [l] BFN
1 AMM - muscle vascular constriction caused by local
VVE - excess blood volume in the veins [l] 0.9915
tissue control [multiplier, ratio to resting state) CLA
ATRRFB ARM - the degree of vasoconstrictor effect of autoregulation in VRA - right atrial volume [l]
RSN BFM
0.9503 VPA - volume in pulmonary arteries [l]
non-muscle and non-renal tissues [multilier, ratio to normal]
VLA - volume in left atrium [l]
AMM RVSM - basal systemic venous multiplier causes basal vascular RBF 1.047
QAO - blood flow in the systemic arteriel system [l/min]
stretch in the venous system [ratio to normal] RSM
0.9625 QVO - rate of blood flow from veins into right atrium [l/min]
AVE - multiplier factor for the effect of the autonomic nervous system 3.082 QPO - rate of blood flow into pulmonary veins and left atrium [l/min] FISFLO 0
4.017 ARM on venous resistance [ratio to basal effect]
RPT BFN - blood flow in non muscle and non renal tissues [l/min]
ANUVN multiplier factor for the effect of angiotensin
2.856 BFM - blood flow in muscles [l/min] 21.04
on venous resistance [ratio to normal] RTP
1 RVSM RBF - renal blood flow [l/min]
SYSTEMIC CAPILLARY PRESSURE PC - systemic caplillary pressure [torr] RR FISFLO - blood flow through a fistula [l/min]
PVS RVSM VT0 4.246
RTP - total systemic peripheral resistance [torr min /l]
2.669 INTPUTS: AV E RV S VT0 - total unstressed blood volume [l]
PVS - average of systemic venous pressure [torr] OUTPUTS: VIM
1.035 VE0 - total excess volume of blood in the vasculature [l] VE0 0.7535
BFN - blood flow in non-renal and non-muscle tissues [l/min] RSN - vascular resistance in non-muscle and non-renal tissues [torr min/l]
BFN 17.67 MCP - mean circulatory pressure [torr]
BFN RVS - resistance in small veins [torr min/l] PC ANUV N RSM - vascular resistrance in muscles [torr min/l]
RVS - resistance in small veins [torr min/l] 0 FIS MCP 7.119
1
FIS
PC Circulatory Dynamics - Flows And Pressures
OUTPUT:
RVS PC - systemic caplillary pressure [torr] 17.67
Resistances in the Systemic Circulation
2.856
Systemic Capillary Pressure

99.85 99.85
99.85
RENAL PERFUSION 142.2 MACULA DENSA
PA PAR
PAR GLOMERULUS
INTPUTS: GFR 0.1246 INTPUTS:
1.047 CNA NAPT1 1.01
PA - systemic arterial pressure[torr] INTPUTS: CNA - Extracellular sodium concentration [mmol/l]
GLB - pressure drop in renal artery RFN GFN - glomerular filtration rate if kidney
0 GBL 1.047 PAR - renal perfusion pressure[torr] 0.1246
caused renal arterial constriction [torr] RFN - renal blood flow if kidney is not damaged [l/min] is not damaged [l/min]
50.07 2 VRC OSA
GLB PVS - average systemic venous pressure [torr] AAR - resistance in afferent arteriole RED CELLS PRODUCTION AND DESTRUCTION
AAR - resistance in afferent arteriole RFN AAR GFN 2.957
[torr min/ll] 0.1246
PVS [torr min/ll] 40 OUTPUTS: 17.67 PC
HM - hematocrit INTPUTS:
50.07 EAR - resistance in efferent arteriole RNAUG1 - macula densa feedback signal VP VP
PPC - plasma colloid osmotic pressure [torr] 47.44 OSA - arterial oxygen saturation [ratio to full saturation]
[torr min/ll] HM [ratio to normal effect] CAPILLARY MEMBRANE FLUID DYNAMICS VB VP 3
91.54 PXTP - back pressurein proximal tubule [torr] GFN RNAUG1 1.05 VP - plasma volume [l]
AAR REK - percent of normal renal function [ratio to normal] 30.53 NAPT1 - delivery of sodium to the macula densa area PPC PPC 30.53 VP
GFLC - glomerular filtration coefficient [l/torr/min] GLP VIM - blood viscosity [ratio to normal blood]
RR [ratio to normal value] -2.687 INTPUTS: 0.0006743 5
RR REK - percent of normal renal function [ratio to normal] RFN - renal blood flow (if kidney is not damaged) [l/min]
41.48 PPC PC - systemic capillary pressure [torr]
PGH VTCLP VTCLP HM REK - fraction of normal kidney mass [ratio to normal]
OUTPUTS: PGH - hydrostatic pressure in the tissue gel [torr] PLASMA PROTEINS DYNAMICS HM VIM
EAR 10.5 PPC - plasma colloid osmotic pressure [torr]
PAR - renal perfusion pressure [torr] OUTPUTS: Macula densa OUTPUTS:
RFN - renal blood flow if kidney is not damaged [l/min] 8 PXTP GLPC 33.45 PTC PTC - colloid osmotic pressure of the tissue gel [torr] INTPUTS:
GFR - glomerular filtration rate [l/min] 12.01 VRC - volume of red blood cells [l]
RBF - renal blood flow [l/min] VTL - rate of return of fluid from the interstitium to the VP - plasma volume [l]
RBF 1.047 PXTP GFN - glomerular filtration rate if kidney is not damaged [l/min] 0.004256 1.152e-005 VB - volume of blood [l]
REK RR - renal resistance [torr min/l] 1.01 blood through the lymph [l/min] VTS DPL VTCLP - rate of leakage of whole plasma through RC1 RFN 1.2
GLP - glomerular pressure [torr] SODIUM EXCRETION HM - hematocrit [%]
0.0208 GLFC VTL TVD - rate of intake of fluid by mounth or otherwise [l/min] the capillary membrane [l/min] DPC 0.1009 RFN
GLPC - average glomerular plasma colloid osmotic pressure [torr] NAPT1 RC1 - red cells production rate [l/min]
0.00119 VUD - loss of fluid into the urine [l/min] DPL - rate of return of protein to the circulation through the lymph [g/min]
GFLC1 PFL - net pressure gradient in glomerulus [torr] INTPUTS: 1.161 RC2 - red cells destruction rate [l/min]
Renal Perfusion PFL 5.991 1.494 NADT DFP - loss of fluid from the pulmonary capillaries [l/min] CPI - concentration of protein in the interstitium [g/l] [torr]
REK NAPT1 - delivery of sodium to the macula densa area TVD VID - rate of transfer of fluid into the cells [l/min] LPPR - rate of production of protein by the liver [g/min] 1.16e-005 RC2 REK 1
1.01 [ratio to normal] CFC - capillary filtration coefficient [l/min/torr] CFILTR 0.003815 CPI PPD - rate of loss of protein through the pulmonary capillary
0.001962 2
THE CONTROL FUNCTIONS OF ANGIOTENSIN 1 RFAB RFAB - the multiplier factor for the effect of renal hemodynamics (normal value CFC=0.01167) membrane [g/min]
0.9714 Glomerulus VUD
NAPT1 on reabsorbtion of sodium and potassium VPN - normal value of plasma volume [l] DPR - rate of loos of protein through the kidney [g/min] Red cells production and destruction
0.001962 2.267e-006
INTPUTS: ANM in the distal tubule collecting duct 0.5803 VTSN - normal value of interstitital fluid volume [l]/n
ANM DTNAI
NAPT1 - delivery of sodium to the macula densa area [ratio to normal] DFP OUTPUTS: OUTPUTs: CPP 72.93
99.85 MYOGENIC AUTOREGULATION OF AFFERENT ARTERIOLE VUDN VUDN - rate of urinary output if kidney is not damaged [l/min] VTC 0.004489 0.03 LPPR
[ratio to normal value] 0.9143 VP - plasma volume [l] PPC - plasma colloid osmotic pressure [torr]
REK - percent of normal renal function [ratio to normal] PAR AMNA - aldosterone for control of sodium reabsorbtion VTS - total interstitial fluid volume [l] LPPR DPC - rate of influx of protein into interstitial fluid from plasma [g/min]
1 REK 40
ANXM - controls of degree of hypertrophy of the juxtaglomerulal INTPUTS: [ratio to normal effect] 0 VID
0.9527 VTCPL - rate of leakage of whole plasma through CPP - plasma protein concentration [g/l]
REK ANU PAR - renal perfusion pressure [torr] AHM - antidiuretic hormone 1
apparatus [0 = no hypertrophy] ANU VID the capillary membrane [l/min] DPL - net rate of protein exchange between liver and plasma [g/min]
PC - capillary pressure [torr] AMNA [ratio to normal effect] NODN 0.1353
ANG - excess of angiotensin concentration caused by infusion CFILTR - rate of filtration from the systemic capillaries [l/min] BLOOD VISCOSITY
MYOGTAU - time delay factor of myogenic response REK - percent of normal renal function [ratio to normal] 0.01167 CFC V PREL 0.9856 PPD
[ratio to normal level of angiotensin] 0 VTC - toral rate of movement of fluid out of systemic capillaries[l/min]
ANUBRM - sensitivity contoller for the effect of angiotensin (in normal condition TENSTC= 240 min) 0.9969 0.5776 DIURET - effect of diuretic on the distal tubule collecting duct CFC
0 ANXM 240 MYOGTAU MYOGRSAA VPR - plasma volume [ratio to normal] INTPUT:
of the baroreceptor system TENSGN - factor of effectiveness of myogenic response [ratio to normal - without diuretics] 3 VPN VTS - total interstitial fluid volume [ratio to normal] DLP -0.007738 HM HM - hematocrit [%] V IM
ANXM MYOGTAU1 AHM
ANUVM - sensitivity controller for the multiplier factor
ANUBR VPN
of the systemic veins NOD 0.1353 V TSREL 1.003 0 DPR OUTPUT:
OUTPUT: 1
1 OUTPUTS: 11.98 VTSN VIM - blood viscosity [ratio to normal]
0 ANG MYOGRSAA - myogenic autoregulation effect on vascular resistance NADT - the normalized delivery of sodium to the distal tubular system DPR
1 TENSGN VTSN
OUTPUTS: in afferent arteriole [multiplier, ratio to normal effect] REK [ratio to normal] Capillary Membrane Fluid Dynamics Plasma Protein Dynamics
ANG TENSG Blood viscosity
ANM - angiotensin multilier factor on vascular resistance [ratio to normal] DTNAI - rate of sodium entry into the distal tubular system [mmol/min]
ANU - angiotensin multilier factor on peripheral ANUV N NODN - sodium excretion rate if kidney is not damaged [mmol/min]
CNU 68.97
arteriolar resistance [ratio to normal] Myogenic Autoregulation of Afferent Arteriole NOD - sodium excretion rate [mmol/min]
0 ANUBRM 1 DIURET CNU - concentration of sodium in urine [mmol/l] 0.24 URFORM
ANUBR - angiotensin multilier factor for the effect in controlling 7.728 UREA
ANUBRM the sensitivity of the baroreceptor system[ratio to normal] 1.494 URFORM
1.047 DIURET
ANUVM - angiotensin multilier factor for the constriction PERITUBULAR CAPILLARIES POT THIRST,DRINKING AND SALT APPETITE INTPUTS: PLURC 4.002
ANC Sodium Excretion
of systemic veins [ratio to normal] ANC 0.7395 URFORM - rate of urea metabolic production [mmol/min]
INTPUTS: INTPUTS: UROD
0 ANUV M ANC - angiotensin concentration in blood [ratio to normal] UROD -rate of urea excretion[mmol/min]
RFN RFN - renal blood flow if kidney is not damaged [l/min] RFAB POT - non-muscle cell PO2 [torr] VTW - total body water volume [l]
ANUVM1 GLPC - average glomerular plasma colloid osmotic pressure [torr] 5.068 AHC1 AHC1 - antidiuretic hormone concentration factor 2.088
STH 0.2387 PLURCNORM - normal value of urea concentration in body fluids [4 mmol/l]
The control Functions of Angiotensin 47.44 POTASSIUM EXCRETION in the circulating body fluids [ratio to normal]
CKE 0.7953 ANM - angiotensin multilier effect to vascular resistance [ratio to normal] V TW
OUTPUTS:
OUTPUTS: 142.2 AMK - effect of aldosterone on potassium secretion [ratio to normal] PLURC - concentration of urea in body fluids [mmol/l]
INTPUTS: KODN 0.06686 ANM PLUR
RFAB - the multiplier factor for the effect of renal hemodynamics DR - forced input of fluid over and above the natural drinking desire 160
0.9803 CNA CKE - extracellular potassium concentration [mmol/l] PLUR - total body urea content[mmol/l]
0.9714 on reabsorbtion of sodium and potassium (it may be used for intravenous infusion as well) [l/min]
1.161 CNA - extracellular sodium concentration [mmol/l] 4 PLURCNORM
GLPC in the distal tubule collecting duct RCPRS 20.65 NADT - the normalized delivery of sodium to the distal tubular system STHENABLED - switching variable:
THE CONTROL FUNCTIONS OF ALDOSTERONE
ANM AMK [ratio to normal] NADT [ratio to normal] 0 DR if STHENABLED<=0, then STH is not calcultated and STH=1 PLURCNORM
RCPRS - renal capillary pressure around the tubular systewm [torr] 0.5803 DTNAI - rate of sodium entry into the distal tubular system [mmol/min] TVDENABLED - switching variable:
INTPUTS: DR Urea
ANM - angiotensin multilier effect to vascular resistance [ratio to normal] if TVDENABLED <=0 then TVD is not calculated and TVD=DR
ANM - angiotensin multiplier effect on vascular resistance DTNAI
5.068 0.9527 AMK - effect of aldosterone on potassium secretion [ratio to normal]
[ratio to normal value] 0.9714
Peritubular Capillaries RFAB - the multiplier factor for the effect of renal hemodynamics 1 STHENABLED TVD
CKE - extracelullar fluid potassium concentrastion [mmol/l] 0.00119
ANM on reabsorbtion of sodium and potassium KOD 0.06686 OUTPUTS:
ALD - rate of infusion of aldosterone STHENABLED
CKE AMNA in the distal tubule collecting duct STH - salt appetite multiplier factor [ratio to normal]
[relative to normal rate of aldosterone secretion] 0.9803
[ratio to normal] TVD - actual rate of fluid intake [l/min]
AMK 1 TV DENABLED
REK - percent of normal renal function [ratio to normal] PGH -2.687
1.494 VUDN - rate of urinary output if kidney is not damaged [l/min] TVDENABLED
OUTPUTS: AFFERENT ARTERIOLE ECF AND ICF ELECTROLYTES AND VOLUMES
40 AARK Thirst, Drinking and Salt Appetite VP VEC 14.98
AMK - effect of aldosterone on potassium secretion [ratio to normal] RFAB
0 ALD AMNA - aldosterone for control of sodium reabsorbtion AMC 0.9783 AARK INTPUTS: PTC 10.5
1 INTPUTS:
AMC - aldosterone concentration [ratio to normal]/n MYOGRSAA AARK - normal resistance in afferent arteriole [torr min/l] OUTPUTS: V TS
ALD VP - plasma volume [l]
RNAUG1 - macula densa feedback signal [ratio to normal] REK KODN - potassium excretion rate if kidney is not damaged [mmol/min] V TS VIC
CKU 34.08 INTERSTITIAL TISSUE FLUIDS, PRESSURES AND PROTEIN DYNAMICS VTS - systemic interstitial fluid volume [l] 24.99
0.9969 AUM - sympathetic vasoconstrictor effect on arteries 0.001962 KOD - potassium excretion rate [mmol/min] VTL 0.004256
VPF - pulmonary interstitial fluid volume [l]
The control Functions of Aldosterone RNAUG1 [ratio to normal] CKU - concentration of potassium in urine [mmol/l]
VUDN INTPUTS: 0.09873 NID - normal rate of sodium intake [mmol/min]
1.05 ANM - angiotensin multiplier effect on vascular resistance AAR V PF
142.2 ANM 50.07 VTS - total interstitial fluid volume [l] STH - salt appetite multiplier factor [ratio to normal] VTW 39.97
[ratio to normal] DPL
0.7953 ANM DPC -rate of influx protein into the interstitial fluid from plasma [g/min] NOD - rate of excretion of sodium in the urine [mmol/min]
CNA THE CONTROL FUNCTIONS OF ANTIDIURETIC HORMONE VIM - blood viscosity [ratio to normal blood]
Potassium Excretion TSP0 - initial value of total interstitial tissue proteins [g] 23.2 KID - rate of intake of potassium [mmol/min]
0.9714 0.1 NID
KOD - rate of excretion of potassium in the urine [mmol/min]
1.167 INTPUTS: AHC1 AUM CPI NID VID -0.001555
AHC1 OUTPUTs: AMK - aldosterone multiplier factor for the effect of aldosterone
CNA - Concentration of sodium in extracelullar fluid [mmol/l] OUTPUT:
1.142 PGH - hydrostatic pressure in tissue gel [torr] on the transport of potassium
AUP AUP - autonomic multipllier effect on ADH hormone excretion etc. AAR - afferent arteriolar resistance [torr l/min] STH
PTC - total colloid osmotic pressure of the tissue gel] through the cell membrane [ratio of normal effect]
[ratio to normal] VIM DPC PTT 1.005 NAE 2131
4.002 VTL - lymph flow rate [l/min] ACLK - sensitivity control of the effect of the aldosterone
0.9714 ANM - angiotensin multiplier effect [ratio to normal]
0.2387 DPL - rate of return of protein to the circulatin by way of the lymph [g/min] on cellular membrane transport
PA - systemic arterial pressure [torr] 1 PLURC UREA AND WATER EXCRETION NOD
Afferent Arteriole CPI - concentration pf protein in the interstitium [g/l] of potassium [ratio of normal effect]
ANM H7 - effect of right atrial volume receptor reflex on ADH PIF -4.683
PTT - total interstitial tissue pressure [torr] VICnorm - normal value of the intracellular fluid volume [l] CNA 142.2
secretion [relative additive factor, normal value = 0] 0.5776 0.1246 INTPUTS: UROD
EFFERENT ARTERIOLE PIF - pressurte in the free interstitial fluid [torr]
99.85 AHMRM - sensitivity coefficient for the effect of ADH PLURC - concentration of urea in body fluids [mmol/l] 0.06 KID
43.333 EARK GFN PTS - solid tissue pressure [torr] OUTPUTS:
on systemic arterial resistance. GFN - glomerular filtration rate if kidney is not damaged [l/min] PTS 5.687
VIF - free interstitial fluid volume[l] KID 0.06686 VEC - volume of extracellular fluid [l]
PA AHM EARK INTPUTS: NADT - the normalized delivery of sodium to the distal tubular system CKE 5.068
AARK - normal resistance in efferent arteriole [torr min/l 0.1353 VG - tissue gel volume[l] VIC - volume of intracellular fluid [l]
[ratio to normal] KOD
0.905 RNAUG1 - macula densa feedback signal TSP - total interstitial tissue proteins [g] VTW - total body water [l]
OUTPUTS: RNAUG1 NODN NODN - sodium excretion rate if kidney is not damaged [mmol/min] VIF 0.6012 0.9803
to efferent arteriole [ratio to normal] VID - rate of fluid transfer between interstitial fluid and cells [l/min]
AHC1 - antidiuretic hormone concentration KODN - potassium excretion rate if kidney is not damaged [mmol/min] KI 3549
ANM EAFRF - sensitivity contoller of macula densa feedback signal 0.06686 278.6 TSP0 NAE - total extracellular sodium content [mmol]
AH7 in the circulating body fluids [ratio to normal] 1 DTNAI - rate of sodium entry into the distal tubular system [mmol/min] VUDN 0.001962 AMK
to efferent arteriole CNA - extracellular sodium concentration [mmol/l]
AHM - antidiuretic hormone multiplier [ratio to normal effect] 0 EFARF EAR 41.48 AHM - antidiuretic hormone [ratio to normal] TSP0 VG 11.41
ANM - angiotensin multiplier effect on vascular resistance CKE - extracellular potassium concentration [mmol/l]
AHMR - effect of antidiuretic on systemic arterial resistance KODN REK - percent of normal renal function [ratio to normal]
EFARF [ratio to normal] KI - total intracellular potassium content [mmol] CKI 142
[ratio to normal effect] 1 ACLK
VIM - blood viscosity [ratio to normal blood] 0.5776 CKI - intracellular potassium concentration [mmol/l]
0 ADH ANUBRM - sensitivity contoller for the effect of angiotensin TSP 278.7 ALCLK
AHRM ANM KCD - rate of transferof potassium from the interstitial fluid
of the baroreceptor system OUTPUTS: 0.001962
ADH AHMR AHM into the intracellular fluid [mmol/min]
ANUVM - sensitivity controller for the multiplier factor AHRM ANM UROD - urea excretion rate [mmol/min] Interstitial Tissue Fluids, Pressures and Gel Dznamics 25 V ICNorm KCD -0.05811
0.9714
of the systemic veins OUTPUT: 1 VUDN - rate of urinary output if kidney id not damaged [l/min] VUD VICnorm
0 AHMRM VIM AAR - afferent arteriolar resistance [torr l/min] VUDN - rate of urinary output [l/min]
AHMRM 1 REK Extracellular and Intracellular Fluid Electrolytes and Volumes
The control Functions of Antitiuretic Hormone Efferent Arteriole
Urea and Water Excretion

Fig 10. Simulink implementation of a Guyton-Coleman model from 1986.

models running in the background can enable students to "play" with this physiological subsystem and
monitor its response to various inputs.
Simulation models in the background of teaching programs are therefore very effective
educational tools that facilitate the comprehension of complex regulation relations in the human
organism and pathogenesis of their malfunction.
From the pedagogical perspective it is advantageous, according to our experiences, if we allow
disconnection of individual regulation loops temporarily, and study reaction of the individual
subsystems separately, which contributes to better understanding of the dynamics of physiological
regulations [12].
During the creation of teaching applications with the use of simulation games, it is necessary, on
one hand, to resolve the creation of the simulation model, and on the other hand the creation of our
own simulator. These are two different tasks, whose effective solution facilitates the use of various
developmental tools [14].
During the creation of simulation models it is advantageous to use developmental tools
designated for creating and identification of simulation models – for example Matlab/Simulink from
the Mathworks company. In this environment, we have also created a special library of physiological
models - Physiology Blockset for Matlab/Simulink, open source software library. 1st Faculty of
Medicine, Charles University, Prague, available at http://physiome.cz/simchips.
Creating simulation models is closely related to issues of creating formalized description of
biological reality, which is the content of the worldwide PHYSIOME project [3, 10].
Creating our own teaching simulators is done in the environment of classic developmental tools
for computer programmers (for example Microsoft Visual Studio, etc.) and tools facilitating the
creation of interactive animated pictures, used in user interface of teaching programs (for example
Adobe Flash, Adobe Flex). The future probably lies in simulators available on the web and on the
accessibility of e-learning educational environment [15, 19]..

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 ISBN 987-80-7080-658-6, CD ROM Proceedings, http://www.humusoft.cz/akce/matlab07
7 From Simulation Games to Medical Simulators
Thirty five years ago, when A. C. Guyton et al. published his large-scale model, the only
possibility to study the behaviour of the model was on large computers that often occupied an entire
room. Nowadays it is possible to run even very sophisticated models on a PC. Moreover, today’s
technology allows us to add on a graphical attractive user-friendly interface to these models.
From the technological standpoint there are no obstacles that would prevent PCs from running
learning simulators for practicing medical decision-making. The basis for a pilot's simulator during
training pilots is the model of the plane. Similarly, one of the prerequisites when creating a medical
simulator is the extensive simulation model of a human organism. This simulation model must include
all significant physiological subsystems – circulation, respiration, kidney function, water, osmotic and
electrolyte homeostasis, acid-base regulation, etc. – which have to be interconnected into the model.
Therefore, now is the time of a renaissance in the formation of large integral models of human
organism, and of the concept of integrative physiology, that Guyton came up with years ago. At the
present time the practical fulfillment is being achieved.
For example, at the present time, Thomas Coleman, one of the co-authors of the legendary
article by prof. Guyton from 1972 [6], together with Guyton’s disciples, created a simulator
Quantitative Human Physiology (QHP), whose theoretical basis is a new mathematical model of
integrative human physiology which contains more than 4000 variables of biological interactions. A
review edition of this simulator is freely available for download at
http://physiology.umc.edu/themodelingworkshop/.
The simulator consists of two software packages.

The first is the equation solver, named QHP 2007.EXE. This is the executable file, prepared for
the Windows operating system (2000, xp, Vista).
The second is an XML document that defines the model, the solution control and the display of
results. This document is distributed over a large number of small files in the main folder and several
subfolders. The XML schema used is described in a preliminary fashion in another section of this
modeling workshop.
The XML document is parsed at program startup. Parsing progress is displayed in the status bar
at the bottom of the program’s main window.
All of the XML files are both machine and human readable. You only need a text editor (such as
Notepad, WordPad).
Unfortunately, the orientation in the structure of such a large model is difficult, due to a large
number of variables (more than 4000).
Standardized notation of the model structure in XML is easily understandable for the machine,
but for a human it is necessary to provide a graphic depiction of the structure of the physiological
regulation relations.
Thus, the suggestions that prof. Guyton et al. sparked, thirty five years ago, by his legendary
article (the concept of integrative physiology, the creation of large-scale models of physiological
subsystems interconnected in an integrative way, and an effort to graphically depict the structure of
physiological regulation relations), nowadays return in a new form and with new possibilities.
References

[1] S. R. Abram, Hodnett, B. L., Summers, R. L., Coleman, T. G., Hester R.L.: Quantitative
Circulatory Physiology: An Integrative Mathematical Model of Human Physiology for medical
education. Advannced Physiology Education, 31 (2), 202-210, 2007.
[2] N. M. Amosov, Palec B. L., Agapov, B. T., Jermakova, I. I., Ljabach E. G., Packina, S. A.,
Solovjev, V. P.: Theoretical Research of Physiological Systems (in Russian). Kiev: Naukova
Dumka, 1977
[3] J. B. Bassingthwaighte: Strategies for the Physiome Project. Annals of Biomedical Engeneering
28, 1043-1058, 2000

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 Technical Computing Prague 2007. 15th Annual Conference Proceedings. Prague, 2007
[4] T. G. Coleman, Randall, J. E.: HUMAN. A Comprehensive Physiological Model. The Physiologist
26, 15-21, 1982
[5] P. Fritzson: Principles of Object-Oriented Modelling and Simulation with Modelica 2.1, Wiley-
IEEE Press, 2003
[6] A. C. Guyton, Coleman T. A. , & Grander H. J.: Circulation: Overall Regulation. Annual Review
of Physiology, 41, 13-41, 1972.
[7] A. C. Guyton, Jones C. E., Coleman T. A.: Circulatory Physiology: Cardiac Output and Its
Regulation. Philadelphia: WB Saunders Company, 1973
[8] A. C. Guyton, Taylor, A. E, Grander, H. J.: Circulatory Physiology II: Dynamics and Control of
the Body Fluids. Philadelphia: WB Saunders Company, 1975.
[9] Guyton A. C.: The Suprising Kidney-Fluid Mechanism for Pressure Control – Its Infinite Gain!.
Hypertension, 16, 725-730, 1990.
[10] P. J. Hunter, Robins, P., Noble D.: The IUPS Physiome Project. Pflugers Archive-European
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[12] J. Kofránek, Anh Vu, L. D., Snášelová, H., Kerekeš, R., Velan, T.: GOLEM – Multimedia
Simulator for Medical Education. In Patel, L., Rogers, R., Haux R. (Eds.). MEDINFO 2001,
Proceedings of the 10th World Congress on Medical Informatics. London: IOS Press, 1042-1046,
2001, available at http://physiome.cz/Guyton.
[13] J. Kofránek, Andrlík, M., Kripner, T., Mašek, J.: From Simulation Chips to Biomedical
Simulator. In Amborski K, Meuth H, (eds.): Modelling and Simulation 2002, Germany 2002,
Proceeding of 16th European Simulation Multiconference, Germany, Darmstadt, 431-436, 2002,
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Biomedical Simulators. The IPSI BgD Transactions on Advanced Research 2. 62-67, 2005,
available at http://physiome.cz/Guyton.
[15] J. Kofránek, Matoušek, S., Andrlík, M., Stodulka, P. Wünsch, Z. Privitzer, P., Hlaváček, J.,
Vacek O.: Atlas of Physiology - Internet Simulation Playground. In Proceedings of EUROSIM
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Ljubljana, MO-2-P7-5, 1-9, 2007, available at http://physiome.cz/Guyton.
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[19] P. Stodulka, Privitzer, P., Kofránek, J., Tribula, M., Vacek, O.: Development of WEB
Accessible Medical Educational Simulators. In Proceedings of EUROSIM 2007, Ljubljana, Vol. 2.
Full Papers (CD). (B. Zupanic, R. Karba, S. Blažič Eds.), University of Ljubljana, MO-3-P4-2, 1-
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Acknowledgement
This research was supported by MŠMT aid grant No. 2C06031 and BAJT servis s.r.o company.

Jiří Kofránek, M.D., Ph.D.

Laboratory of Biocybernetics,
Dept. of Pathophysiology,
1st Faculty of Medicine,
Charles University, Prague
U Nemocnice 5, 128 53 Praha 2,
Czech Republic
e-mail: [email protected]

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